General Medicine ,Dentistry Second Term

8/10/2019 General Medicine ,Dentistry Second Term

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II. General medicine lectures fordentistry students.

Second term

Cardiology

1-Rheumatic fever:

An acute inflammatory complication of group A streptococcal

infection, with a possiility of residual heart disease as a result ofcarditis. It occurs most often in children !streptococcal sore throat is

common" , the pea# age-related incidence is etween $ and 1$ years.

%he disease is more common among population with low social and

economic standards, due to overcrowding.

&athogenesis:Rheumatic fever follows acute eta-hemolytic streptococcal infection

!group A" of the pharyn'.

%he mechanism of development of rheumatic fever after infection is

still un#nown.

%he hypothesis of (antigenic mimicry( etween heart valves and

myocardial cells with acterial antigens was suggested, anormal

immune response y the human host to these antigens, will result in

damage to the cardiac tissue. Genetic predisposition may e

involved.

)iagnosis of rheumatic fever*linical diagnosis is the main method of diagnosis supported y

laoratory evidence of streptococcal infection. laoratory tests may

help in the diagnosis of R+ ut all of them are non-specific.

*riteria of diagnosis: ! Updated Jones criteria"

aor criteria: $ criteria


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1. *arditis.

. igratory polyarthritis.

/. Sydenham0s chorea !Rheumatic chorea".

. Sucutaneous nodules.

$. 2rythema marginatum.

inor criteria:

1. +ever.

. Arthralgia.

/. 2levated acute phase reactants ! c- reactive proteins".

. &rolonged &-R interval in 2*G.

$. 2vidence of a recent streptococcal infection !AS3%, %hroat

culture".

At least 456 of patients with acute R+ have an elevated anti-

streptolysin-3 titer at presentation.

%o diagnose Rheumatic fever: According to 7ones criteria. 2ither:

maor criteria.

one maor 8 two minor criteria. &lus evidence of an recent streptococcal infection for oth.

1- *arditis:

&ancarditis involving the pericardium, myocardium, and

endocardium. *linical manifestations includes: Sinus tachycardia,

the murmur of mitral regurgitation, an S/ gallop, a pericardial

friction ru, and cardiomegaly, and may e evidence of heartfailure. 2*G may show prolonged &-R interval.

3utcome of rheumatic carditis:

9ealing of the rheumatic valvulitis may cause firous thic#ening

and adhesion, resulting in the most serious complication of

rheumatic fever, valvular stenosis andor regurgitation of the valve.


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%he mitral valve is involved most fre;uently, followed y the aortic

valve.

)iseased valve is susceptile to acterial endocarditis.

- igratory polyarthritis:

+ound in


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1. Antiiotics %herapy immediately: a complete 15-day

course in adults of :

3ral penicillin > !$55 mg twice daily".

2rythromycin !$5 mg four times daily" for those with penicillin

allergy.

?en@athine penicillin G !a single intramuscular inection of 1.

million units" may e used to prevent coloni@ation in the throat.

. Salicylates for rheumatic arthritis: Given in increasing doses

up to g four times daily. +or to wee#s and gradually tapered

to prevent reound.

/. &rednisone ! *orticosteroids" for rheumatic carditis in doses

up to /5 mg four times daily in severe cases, as the patient

improves, salicylates can e added during the tapering of the

steroid doseB this may re;uire to wee#s.

Secondary prophyla'is:

!According to American 9eart Association and of the Corld 9ealth 3rgani@ation."

%o prevent suse;uent coloni@ation of the upper respiratory tract

with group A streptococci, and prevent recurrence of rheumatic fever.

?en@athine penicillin G !Intramuscular", 1. million units every

wee#s.

&enicillin > !$5 mg twice daily" orally.

Sulfadia@ine !1.5 g daily" orally.

)uration of prophylactic treatment:

Should e individuali@ed ut at least for $ years.

9igh ris# group may e for life !patients with rheumatic heart

disease".

3utcome of Rheumatic fever:

*omplete healing.

Residual damage to the heart valves.


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%he heart may escape the first attac# of rheumatic feverwithout residual damage, ut rarely escapethe secondattac#, so prophylactic treatment is mandatory after the firstattac#.

.>alvular heart diseases:

itral stenosis !S":

2tiology:

%wo-thirds of all patients with mitral stenosis !S" are females. It is

generally rheumatic in origin !post-rheumatic fever". It is rarely

congenital. &ure or predominant S occurs in appro'imately 5 6 of

all patients with rheumatic heart disease.

&athology:

%he valve leaflets are thic#ened y firous tissue, the mitral

commissures fuse, the chordae tendineae fuse and shorten, the

valvular cusps ecome rigid, leading to narrowing at the ape' of the

funnel-shaped valve, sometimes calcific deposits occur in the valve.

*linical picture:

Chen the mitral valve is stenosed more than /56, a significant rise

of the intra-atrial pressure occurs trying to force the lood into the

left ventricle to maintain the cardiac output.

%his rise in pressure eventually will e reflected on the pulmonary

circulation and on the right side of the heart leading to symptoms.

1.2'ertional dyspnea:

%he first symptom to appear. %he more tight the valve, the lesser the

e'ertion needed to cause dyspnea.

Dormally during e'ertion, lood flow from the left atrium to the left

ventricle increases, ut in S, lood accumulates in the left atrium

and pulmonary veins leading to pulmonary congestion and dyspnea.

.&aro'ysmal nocturnal dyspnea:


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)igitalis glycosides may help patients with A+ to slow the ventricular

rate. ?eta loc#ers may help.

*ontinuous anticoagulants for prolonged cases to prevent emolism.

Surgery: +or severe cases, either valvotomy or valve replacement.

itral regurgitation:

2tiology:1. sually rheumatic, R is more common in males contrary to S.

. itral valve prolapse.

/. *ongenital.

. &apillary muscle rupture post acute myocardial infarction.

$. *hest trauma, due to spontaneous rupture of chorda tendineae.

. Acute R: In acute infective endocarditis.

Symptoms and signs of R :

Dormally the mitral valve closes during ventricular systole to prevent

regurgitation of lood into the left atrium, and allow the lood to flow

only in the aorta.

In R, the valve is defective allow the lood to flow ac# into the left

atrium causing ac# pressure on the pulmonary circulation and

pulmonary congestion.

1. &alpitation: awareness of heart eats due to e'cess ventricular

filling due to regurgitant lood from the left atrium.

. )yspnea: due to pulmonary congestion.

/. 2molism is possile with atrial firillation.

*ardiac e'amination: &an-systolic murmur on the mitral area

radiating to the a'illa.

)iagnosisE treatment:

)iagnosis: same as S.


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9istory E e'amination.

F-ray chest: may e normal until heart failure occur.

2*G: Heft ventricular hypertrophy.

2chocardiography.

*ardiac catheteri@ation.

%reatment of AS

1. &rophyla'is against I2, rheumatic activity.

. In patients with severeAS, strenuous physical activity

should e avoided even in the asymptomatic stage.

/. )igitalis glycosides, sodium restriction, and the cautious

administration of diuretics are indicated in the treatment of

congestive heart failure.

. Surgery is preferred to avoid sudden death : >alve

replacement.

Aortic regurgitation:

2tiology:

&ure or predominant AR are males, females predominate among

patients with AR who have associated mitral valve disease.

ost cases are rheumatic in origin.

Acute AR also may result from infective endocarditis, which can

develop on a valve previously affected y rheumatic disease.

*ongenital stenosis.

&athogenesis:

Dormally the aortic valve closes at the end of ventricular systole

to avoid regurgitation of lood ac# to the left ventricle to

maintain perfusion to the different tissues.

?ut in AR the valve does not close allowing lood to flow ac# to

the left ventricle together with lood coming normally from the left


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atrium, volume overload occur and ventricular dilatation occur.

%he left ventricle have to pump e'tra-volume of lood it receives

resulting in hyperdynamic circulation and ig volume pulse, and

many other peripheral signs.

Symptoms:

&atients with severe AR may remain asymptomatic for 15 to 1$ years.

&alpitation !awarness of heart eats", may persist for years efore

dyspnea occur.

2'ersional dyspnea.

3rthopnea, paro'ysmal nocturnal dyspnea, and chest pain.

Signs:

9igh pulse volume.

9yper#inetic cardiac ape'.

2arly diastolic murmur on the second aortic area.

)iagnosis and treatment of AR:

Same as AS.

Infective endocarditis !I2"

A serious complication to valvular heart disease either rheumatic or

congenital. %he most common organism causing I2 is streptococcus

viridans, S. fecalis. Chich are normal commensals in the oral cavity.inor procedures ! dental e'traction " may result in actremia,

settling on the valve and cause endocarditis.

Symptoms:

Symptoms of I2 include prolonged fever usually /J degrees,

mar#ed to'emia !anaemia, anore'ia, and weight loss".


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&eripheral emolisation in different organs !#idneys causing

hematuria, s#in, eyes".

Splenomegaly.

%reatment of I2:

+or streptococcus viridans:

&enicillin G 23 million units IV / 4hfor wee#s.

3R:

&enicillin G 3 million units IV / 4h + gentamicin1 mg/kg

IM or IV / 8h, both for 2 Weeks.

&rophyla'is of I2:

Should e given for any patient with rheumatic or congenital

valvular lesions efore any surgical procedure especially in the

mouth.

+or oral cavity, respiratory tract, or esophageal procedures:

1. Standard regimen:

Amo'icillin g orally 1 hour efore procedure.

. Inaility to ta#e oral medication:

Ampicillin g I> or I within /5 min of procedure.

/. &enicillin allergy:

larithrom!cin "## mg orall! 1 h before

$roce%ure. e$hale&inor cefa%ro&il2.# g orall! 1 h before

$roce%ure.

. &enicillin allergy 8 Inaility to ta#e oral medication: *efa@olin 1 g I> or I /5 min efore procedure.

Ischemic heart disease

)efinition:


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Ischemia is lac# of o'ygen due to inade;uate perfusion, which

results from an imalance etween o'ygen supply and demand.

%he most common cause of myocardial ischemia is

atherosclerotic disease of coronary arteries.*auses of myocardial ischemia:

1. Atherosclerosis of coronary arteries.

. Arterial thromosis.

/. *oronary spasm.

. Severe ventricular hypertrophy !hypertension or aortic stenosis"

due to relative increase in o'ygen demands. 3r decreased o'ygen

in lood as in severe anemia.$. *oronary emolism !Rare".

D.?: A comination of causes is possile.

*oronary atherosclerosis:

Ris# factors: Anormal lood lipids, cigarette smo#ing,

hypertension, and diaetes mellitus.

%hese factors leads to suintimal collections of anormal fat,

cells, and deris !atherosclerotic pla;ues", leading to narrowing

of coronary lumen

Symptoms:

1. Angina pectoris:

$5- to 5-year-old man or $- to


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*igarette smo#ing.

2'posure to cold.

9eavy meals.

Anginal pains are relieved y rest.

Angina occurring at rest is called unstale angina.

)iagnosis:

%he typical history of pain is diagnostic.

2*G: %ypical changes during pain.

Stress test: Recording 2*G changes during e'ercise.

Stress myocardial perfusion: imaging after the intravenous

administration of a radioisotope such as thallium 51 or

technetium JJm.

%wo-dimensional echocardiography of the left ventricle to

assess wall motion anormalities due to myocardial infarction or

persistent ischemia.

*oronary Arteriography: %o map out the coronary

circulation especially efore surgery.

Haoratory and F-ray investigations:

?lood sugar to e'clude diaetes mellitus.

Serum creatinine for renal disease, since ) and renal failure may

accelerate atherosclerosis.

?lood lipids !cholesterol, low density, and high density".

F-ray chest: Aortic calcification, cardiac si@e.

%reatment:

1. Explanationand reassurance.


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. Identification and treatment of aggravating conditions and risk

factors:

3esity, hypertension, hyperthyroidism, anormal lipids, cigarette

smo#ing, ).

/. Adaptation of activity:%ry to adapt his activity to prevent the pain,

avoid anger, fre;uent meals.

D.?: *igarette smo#ing accelerates coronary atherosclerosis in oth

se'es and at all ages and increases the ris# of myocardial infarction

and death. ?y increasing myocardial o'ygen needs and reducing

o'ygen supply it aggravates angina.

. )rug therapy:

Ditrates: It causes systemic venodilation, therey reducing

myocardial wall tension and o'ygen re;uirements, and dilating the

coronary vessels andincreasing lood flow in collateralvessels.

%here are short acting SH nitrates and long acting talets.

?eta-loc#ers: &ropranolol, reduce myocardial o'ygen demand

!inhiiting the increases in heart rate and myocardial contractility".

*alcium antagonists: Difedipine, and verapamil.

%hey reduce cardiac o'ygen demand, dilate coronary arteries.

Aspirin:

Anti-platelet aggregator, protect against ischemia especially post

infarction.

Acute yocardial infarction

I occurs if sudden decrease in coronary lood flow following a

thromotic occlusion of a coronary artery previously narrowed y

atherosclerosis.

*linical presentation:


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In aout $56 of patients there is a precipitating factor as vigorous

physical e'ercise, emotional stress, or a medical or surgical

illness.

1. Severe chest pain descried as heavy, s;uee@ing, and crushing isthe most common symptom.

Site is central chest andor the epigastrium, sometimes it radiates

to the arms.

Hess common sites of radiation include the adomen, ac#, lower

aw, and nec#.

sually accompanied y wea#ness, sweating, nausea, vomiting,

an'iety, and a sense of impending death.

2'amination:

&atients are an'ious and restless, trying to relieve the pain y

moving aout in ed, altering their position, and stretching.

&allor is associated with perspiration and coolness of the

e'tremities.

ay e changes in lood pressure, and pulse.

Investigations:

1. 2*G: %ypical changes in S% segment and KRS comple'.

. Serum cardiac mar#ers:

*reatine phospho#inase !*L": rises within to 4 h and generally

returns to normal y 4 to


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. yocardial perfusion imaging with thallium 51 or technetium

JJm: Reveal a cold spot.

%reatment:

1. &re-hospital care: rapid transfer to the hospital with a trained

team capale of resuscitative maneuvers, including defirillation.

. 9ospital management:

Emergency treatment:Aspirin, o'ygen inhalation, SH nitrates,

Intravenous eta loc#ers andmorphine to control pain.

Decrease infarct size:

%hrompolysis: sing tissue plasminogen activator !t&A", or

strepto#inase intravenously. &ercutaneous %ransluminal *oronary Angioplasty !&%*A": *an

also decrease infarcted area.

Drug therapy:

9eparin: anticoagulant.

?eta-loc#ers.

%reatment of complications:

Arrhythmia.

*ardiogenic shoc#.

9ypertension

1. Arterial hypertension:

2levation of systolic andor diastolic lood pressure, eitherprimary or secondary.

Chen hypertension is suspected, lood pressure should e measured at

least twice during two separate e'aminations after the initial screening.

*lassification of lood pressure in adults:

(Nollenberg NK, summary of the joint national committee and WHO and international society of

hypertension 1995!


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Dormal lood pressure:

Systolic 1/5

)iastolic 4$ mmhg.

9igh normal lood pressure:

Systolic 1/5 M 1/J mm hg

)iastolic 4$ M 4J mm hg

ild hypertension: stage 1

Systolic 15 M 1$J mm hg

)iastolic J5 M JJ mm hg

oderate hypertension: stage

Systolic 15 M 1ery severe hypertension: stage

Systolic N 15

)iastolic N 15.

orderline isolated systolic hypertension: )iastolic ?& is J5 mm9g,

systolic ?& etween 15 and 1$J.

Isolated systolic hypertension: )iastolic ?& is J5 mm9g, Systolic ?&

is N 15 mm9g.

Haile hypertension:

&atients who are sometimes, ut not always, have arterial pressures in

the hypertensive range. %hey are considered to have orderline ?&.


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alignant hypertension: lood pressure aove 5515, the condition is

defined y the presence of papilledema, usually accompanied y retinal

hemorrhages and e'udates, rather than y the asolute pressure level.

&atient evaluation:

9istory, physical e'amination.

Symptoms: ost patients with hypertension have no specific

symptoms, identified only in the course of a physical e'amination. Chen

symptoms occur, it may e related to:

1- %he elevated pressure itself , headache only in severe hypertension in

the occipital region , present in the morning susides spontaneously

after several hours.

3ther complaints that may e di@@iness, palpitations, easy

fatigaility, and impotence.

- %he hypertensive vascular disease, epista'is, hematuria, lurring of

vision owing to retinal changes, episodes of wea#ness or di@@iness

due to transient cereral ischemia, angina pectoris, and dyspnea

due to cardiac failure. &ain due to dissection of the aorta or to alea#ing aneurysm is an occasional presenting symptom.

/- %he underlying disease, in the case of secondary hypertension.

2'amination of the patient: ainly to reveal secondary causes of

hypertension, as endocrinal causes, renovascular occlusion.

Haoratory tests:?asic initial evaluation: rine analysis, lood sugar, serum creatinine,

lood lipids, and 2*G.

Screening for secondary hypertension: +or renovascular hypertension,

*ushing=s syndrome, and pheochromocytoma

A. &rimary or essential hypertension !29"


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renal insufficiency. %hus, even in its mild forms, hypertension is a

progressive and lethal disease if left untreated.

%he heart: 9ypertrophy, enlargement and finally heart failure.

%he retina: retinal changes include narrowing of the arterioles, as well

as the appearance of hemorrhages, e'udates, and papilledema resulting

in scotomata, lurred vision, and even lindness, if the changes are in

the macular area.

%he *DS: Include vascular occlusion causing cereral infarction is

secondary to the increased atherosclerosisB cereral hemorrhage is the

result of oth the elevated arterial pressure and the development of

cereral vascular microaneurysms.

%he #idney:

*hanges in the glomerular capillaries, causing proteinuria, hematuria

and lastly renal failure.

%reatment:

General measures:!1" relief of stress.

!" dietary management: Reduce sodium, calory , and saturated fats.

!/" regular aeroic e'ercise.

!" weight reduction !if needed".

!$" control of other ris# factors contriuting to the development of

arteriosclerosis.

)rug therapy:

1- )iuretics: Acts through depletion of plasma volume

! %hia@ides, spironolactone".

- Antiadrenergic agents: alpha-receptor agonists. Stimulation of

alphareceptors in the vasomotor centers of the rain reduces

sympathetic outflow agents !clonidine, methyldopa".

/- Alpha-Adrenergic Receptor ?loc#ers: loc#ing sympathetic

receptors P1 and P in the *DS! pra@ocin".


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- ?eta-Adrenergic Receptor ?loc#ers: loc# sympathetic effects

on the heart , reducing cardiac output, lowering arterial

pressure when there is increased cardiac sympathetic nerve

activity !cardioselective ?1 loc#er:atenolol ", ! &ropranolol:

non-selective".

$- >asodilators: Arteriolar vasodilators: Reduce peripheral

resistance !9ydrala@ine".

- A*2 inhiitors: &revent production of angiotensin !potent

vaso-constrictor", preserve rady#inin !vaso-dilator",

!*aptopril".


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/. Anormalities of the heart valves in which the heart muscle is

damaged y the long-standing e'cessive hemodynamic urden

imposed y the valvular anormality, and rheumatic process.

. 9ypertension: causing left ventricular overload.

&recipitating causes of heart failure:

1. infection: &atients with pulmonary vascular congestion are also more

susceptile to pulmonary infections, any infection in a predisposed

patient may lead to heart failure.

. Anemia: defective o'ygenation is compensated y increase in the

cardiac output, which can e maintained y a normal heart, ut not a

diseased heart.

/. %hyroto'icosis and pregnancy: as in anaemia, oth conditions lead

to increased cardiac output.

. Arrhythmias. In patients with compensated heart disease,

tachyarrhythmia reduce ventricular filling. In patients with ischemic

heart disease, it also cause ischemic myocardial dysfunction.

$. Rheumatic and other forms of myocarditis.

. Infective endocarditis.


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. 9igh output failure: *3& is increased as in thyroto'icosis, and

anemia.

$. Heft sided failure: when the left ventricle cannot pump lood, it

accumulates ehind in the pulmonary circulation resulting in

dyspnea and orthopnea as a result of pulmonary congestion.

. Right sided failure: when the right ventricle is affected as in

pulmonary hypertension, symptoms are usually those of systemic

venous congestion: lower lim edema, congestive hepatomegaly.

?iventricular failure: Chen oth ventricles fail. Giving rise to symptoms

of oth sides, it occurrs due to a myocardial disease affecting oth

ventricles simultaneously, or left sided failure followed later y right

sided failure due to pulmonary hypertension. As in aortic valve disease.

Symptoms of heart failure:

1. )yspnea"

Respiratory distress that occurs as the result of increased effort in

reathing is the most common symptom of heart failure.

. 3rthopnea: )yspnea in the recument position is usually a late

manifestation of heart failure.

/. &aro'ysmal !nocturnal" )yspnea: Severe shortness of reath and

coughing that generally occur at night, usually awa#en the patient

from sleep, relieved y sitting in ed.

. +atigue, Cea#ness, And Adominal Symptoms: Anore'ia and

nausea associated with adominal pain and fullness are fre;uent

complaints and may e related to the congested liver and portal

venous system.

&hysical e'amination:

1. Sinus tachycardia, cardiac enlargement.

. *yanosis of the lips and nail eds, the patient may insist on sitting

upright !3rthopnea".


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!" )ilated cardiomyopathy.

!c" yocardial depression in septic shoc#.

ii" echanical:

!a" itral regurgitation.

!" >entricular septal defect.

" 2'tracardiac ostructive shoc#:

i" *ardiac tamponade.

ii" assive pulmonary emolism.

/" 9ypovolemic shoc#:

i" 9emorrhage.

ii" +luid depletion.

" )istriutive shoc#:

i" Septic shoc#.

ii" )rug overdose.

iii" Anaphylactic.

iv" Deurogenic.

v" 2ndocrinological.

9ypovolemic shoc#:

Reduction in circulating lood volume, which decreases preload and

leads to inade;uate ventricular filling, the result is decreased stro#e

volume and inade;uate cardiac output. 9ypovolemic shoc# may result

from hemorrhage or from fluid depletion due to vomiting, diarrhea,

urns, or dehydration. 9ypovolemic shoc# is the most common type

seen clinically.

Hoss of 156 of total lood volume is corrected y compensatory

mechanisms that improve ventricular filling and *3&, and

maintain ?&:


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1. Sympathetic discharge and adrenal release of catecholamines, leads

to arterial vasoconstriction, augmented venous return, and

tachycardia.

. Reduction of hydrostatic pressure in the peripheral capillaries favors

transudation of fluid from the e'tracellular space into the vessels.

/. Intravascular volume contraction leads to activation of the renin-

angiotensin system, increased release of antidiuretic hormone

!A)9", and elevated levels of A*%9 and aldosterone.

Chen 5 to $ 6 of the lood volume is lost rapidly, the

compensatory mechanisms egin to fail and the clinical shoc#

syndrome occurs. *ardiac output declines, and there is

hypotension despite generali@ed vasoconstriction, followed y

end organ damage.

*ardiogenic shoc#:

Severe depression of cardiac performance. 9emodynamically, it is

characteri@ed y a systolic lood pressure 45 mm9g. %he most

common cause is myocardial infarction with loss of 5 6 or more of the

left ventricular mass.

2'tracardiac ostructive shoc#:

*ardiac tamponade: *auses increased pericardial pressure which

impairs ventricular diastolic filling, decrease preload, stro#e volume,

and cardiac output.

assive pulmonary emolism: Also results in right sided failure, and

decreased left ventricular filling.

)istriutive shoc#:

*aused y peripheral vasodilatationB although cardiac output may e

normal or high, organ and tissue perfusion pressures are inade;uate.


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Septic shoc# is an e'ample of this type of shoc#B other causes include

anaphyla'is, neurogenic and adrenal insufficiency.

Septic shoc#:*aused y severe acterial infection, acteria circulating in the lood

releases acterial to'ins, which is a potent stimulator of cyto#ines and

mediators release such as histamine and #inines and others , causing

peripheral vasodilatation which causes hypotension, and myocardial

depression leading to reduction in cardiac output, organ system failure

occur then death follows if not corrected.

ortality in untreated cases is aout $56.

Anaphyla'is:

Hife-threatening anaphylactic response of a sensiti@ed human after

e'posure to a specific antigen, and is manifested y respiratory distress

often followed y vascular collapse or y shoc#, cutaneous

manifestations include prurites and urticaria, with or without

angioedema are characteristic of such systemic anaphylactic reactions.Gastrointestinal manifestations include nausea, vomiting, crampy

adominal pain, and diarrhea.

aterials causing this reaction are numerous:

)rugs !insulin, penicillin, cephalosporins, amphotericin ?,

nitrofurantoin", insect ites, food !eggs, seafoods, nuts, grains and

eans", local anesthetics !procaine and lidocaine".

*linically: Symptoms appear seconds to minutes after introduction of

the antigen, generally y inection or less commonly y ingestion. %here

may e upper or lower airway ostruction or oth. Haryngeal edema may

e e'perienced as a (lump( in the throat, hoarseness, or stridor, chest

tightness and ronchial spasm, urticarial eruptions are intensely pruritic

and may e locali@ed or disseminated. %hey may coalesce to form giant

hives.

A locali@ed, nonpitting, deeper edematous cutaneous process,

angioedema may occur.


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&atients may die of vascular collapse due to peripheral vasodilatation,

and critical reduction of lood volume.

*linical picture of shoc#:Shoc# is characterised y hypotension, which in adults generally refers

to a mean arterial pressure elow 5 mm9g.

3ther signs and symptoms include tachycardia, oliguria, a clouded

sensorium, and cool, mottled e'tremities indicative of reduced lood

flow to the s#in. etaolic acidosis, often due to elevated lood lactate

levels, reflects prolonged inade;uate lood flow to tissues.

3ther clinical manifestations are specific to the type of shoc#. &atients

with hypovolemic shoc# fre;uently have a history of gastrointestinal

leeding, hemorrhage from another site, or clear evidence of large

volume losses via diarrhea andor vomiting.

&atients with cardiogenic shoc# usually have symptoms and signs of

heart disease, mechanical causes of cardiogenic shoc# fre;uently cause

heart murmurs, such as those of mitral regurgitation, aortic stenosis, or

ventricular septal defect. &atients with septic shoc# there may e

evidence of locali@ed infection as well as fever and chills.

%reatment:1. Shoc# is an emergency situationB the patient should e managed in

intensive care unit. *ontinuous electrocardiographic monitoring

should e performed for detection of rhythm disturances.

. +re;uent measurements of arterial lood gases, serum electrolytes,complete lood counts, and coagulation parameters should e done

to follow the patient=s progress and to monitor the effects of therapy.

/. %he main goal of treatment is to maintain mean arterial pressure, and

to ensure ade;uate perfusion and delivery of o'ygen and other

nutrients to the vital organs.

. 9ypovolemic shoc#: infusion of fluid is the fundamental treatment of

acute hypovolemia, infusion of crystalloid solutions !saline" or


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colloid solutions !alumin", or lood transfusion in hemorrhagic

shoc#.

$. *ardiogenic shoc#: If due to myocardial infarction, attention should

e directed to reducing myocardial ischemia, y supplemental

o'ygen, and administration of intravenous nitroglycerin if ?& allows,

up to even emergency coronary angioplasty. )opamine and

analogues may e useful as enotropic agents.

. Septic shoc#: %reat infection y surgical drainage andor antiiotic

therapy, o'ygen inhalation, lood and fluid transfusion to

maintenance tissue o'ygen delivery.


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) is the most common endocrine disease worldwideB it is

characteri@ed y metaolic anormalities and y long-term

complications involving the eyes, #idneys, nerves, and lood vessels.

*haracteri@ed y hyperglycemia, either due to reduced insulin secretion,

decreased glucose usage, and increased glucose production.

Action of insulin:

Insulin is the most important regulator of the alance etween hepatic

glucose production and peripheral glucose upta#e and utili@ation.

In the fasting state, low insulin levels promote hepatic gluconeogenesis

and glycogenolysis to prevent hypoglycemia. How insulin levels

decrease glycogen synthesis, reduce glucose upta#e in insulin-

sensitive tissues, and promote moili@ation of stored precursors. %hese

processes are of critical importance to ensure an ade;uate glucose

supply for the rain.

&ostprandially, a large glucose load elicits a rise in insulin and fall in

glucagon, leading to a reversal of these processes. %he maor portion of

postprandial glucose is utili@ed y s#eletal muscle.

*lassification of ):

I. &rimary:1. %ype 1: Insulin dependent ): ? cell destruction !A-immune

mediated E ?- Idiopathic".

. %ype : Don-insuline dependent: Insuline rTsistant diaetesmellitus.


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II. Secondary:

1 !ancreatic disease

" #ormonal a$normalities

% Chemical induced dia$etes

& 'nsulin receptor a$normalities

( Dia$etes )ith genetic syndromes

&athogenesis of type 1A ! I))": Immune mediated type 1:

Autoimmune destruction of the eta cells of the pancreas, triggered y

an environmental factor !viral infection", which is followed y

autoimmune inflammation and gradual destruction of the eta cells with

time, insuline levels drop until it is not enough to control lood sugar,

then clinical disease appears.

%he stage in which the patient is not symptomati@ing during active

inflammation is termed prediaetes.

%he role of inheretance in this type of diaetes is still unclear.

&revention of %ype 1A ):

%heoretical adminstration of immunosuppressive drugs to reduce ? cell

destruction at an early stage, may prevent the disease.

&athogenesis of type ):

%ype ) has a strong genetic component, there is a strong familial

predisposition, this type is characteri@ed y impaired insulin secretion,

peripheral insulin resistance, and e'cessive hepatic glucose production.

3esity, particularly visceral or central, is very common in type ).

&revention of type ): Hife-style modifications have een

suggested to prevent or delay its onset. Individuals with a strong family

history or those at high ris# for developing ) should e strongly

encouraged to maintain a normal ody mass inde' and to engage in

regular physical activity.


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*linical picture of ):

Symptoms of hyperglycemia include polyuria, polydipsia, weight loss,

fatigue, wea#ness, lurry vision, fre;uent superficial infections

!vaginitis, fungal s#in infections", and slow healing of s#in lesions after

minor trauma. etaolic derangements relate mostly to hyperglycemia

!osmotic diuresis, reduced glucose entry into muscle" and to the

cataolic state of the patient !urinary loss of glucose and calories,

muscle rea#down due to protein degradation and decreased protein

synthesis". ?lurred vision results from changes in the water content of

the lens and resolves as the hyperglycemia is controlled.

&hysical e'amination:

+ull e'amination with special attention to weight or ody mass inde',

retinal e'amination, orthostatic lood pressure, foot e'amination,

peripheral pulses, and insulin inection sites.

*areful e'amination of the lower e'tremities should see# evidence of

peripheral neuropathy, calluses, and superficial fungal infections. Dail

disease, and foot deformities in order to identify sites of potential s#in

ulceration.

>iratory sensation, and the aility to sense touch, is useful to detect

moderately advanced diaetic neuropathy.

Since dental disease is more fre;uent in ), the teeth and gums should

also e e'amined.

&atients with type 1 ) tend to have the following characteristics:!1" 3nset of disease efore the age of /5 years.

!" Hean ody.

!/" Re;uirement of insulin as the initial therapy.

!" Hiaility to develop #etoacidosis.

!$" An increased ris# of other autoimmune disorders such as

autoimmune thyroid disease, adrenal insufficiency, pernicious anemia,

and vitiligo.


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In contrast, &atients with type ) often have the following features:

!1" )evelop diaetes after the age of /5.

!" Are usually oese !456 are oese, ut elderly individuals may e

lean".

!/" ay not re;uire insulin therapy initially.

!" ay have associated conditions such as insulin resistance,

hypertension, cardiovascular disease, dyslipidemia, or polycystic ovary

syndrome.

In type ), insulin resistance is often associated with adominal

oesity !as opposed to hip and thigh oesity" and hypertriglyceridemia.

Haoratory assessment:

*riteria of diagnosis of ) are:

1. +asting !overnight": >enous plasma glucose concentration 1

mgdH on at least two separate occasions.

. %wo-hour plasma glucose concentration 55 mgdH during oral

glucose tolerance test.

/. Random lood sugar 55 mgdH 8 symptoms of diaetes

!polyuria, polydipsia, and weight loss"

D.?: If the hours reading is one 55 mgdH, and the other is

etween 15 and 55 mgdH, the diagnosis is impaired glucose

tolerance.

%he patient should e screened for )-associated conditions !e.g.,

microaluminuria, dyslipidemia, thyroid dysfunction". Individuals

at high ris# for cardiovascular disease should e screened for

asymptomatic coronary artery disease y appropriate cardiac

stress testing, when indicated.

%reatment of ):

%he goals of therapy for type 1 or type ) are to:

!1" 2liminate symptoms related to hyperglycemia.


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!" Reduce or eliminate the long-term microvascular and

macrovascular complications of ).

!/" Allow the patient to achieve as normal a life-style as possile.

%o achieve this goal we need:

&atient education aout ):

Self-monitoring of lood glucose, using plasma glucose

assessment and glycated hemogloin or !9A1c".

rine #etone monitoring !type 1)"B

Insulin administrationB

Guidelines for diaetes management during illnessesB

anagement of hypoglycemiaB

+oot and s#in careB

)iaetes management efore, during, and after e'erciseB

Ris# factor-modifying activities.

Dutrition:

edical nutrition therapy !D%" is a term used y the American

)iaetes Association !A)A" to descrie the optimal coordination of

caloric inta#e with other aspects of diaetes therapy !insulin, e'ercise,

weight loss". 9istorically, nutrition has imposed restrictive, complicated

regimens on the patient. *urrent practices have greatly changed,

though many patients and health care providers still view the diaetic

diet as monolithic and static. +or e'ample, modern D% now includes

foods with sucrose and see#s to modify other ris# factors such as

hyperlipidemia and hypertension rather than focusing e'clusively on

weight loss in individuals with type ).

%he maority of type ) individuals are oese, and weight loss is still

strongly encouraged and should remain an important goal. edical

treatment of oesity is a rapidly evolving area.

2'ercise

2'ercise is an integral component of diaetes care that can have

multiple positive enefits !cardiovascular enefits, reduced lood


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pressure, maintenance of muscle mass, reduction in ody fat, weight

loss, etc.". +or individuals with type 1 or type ), e'ercise is also

useful for lowering plasma glucose !during and following e'ercise" and

increasing insulin sensitivity.

%ype 1 )iaetes ellitus"

%he goal is to design and implement insulin regimens that mimic

physiologic insulin secretion. ?ecause individuals with type 1 ) lac#

endogenous insulin production, administration of asal, e'ogenous

insulin is essential for regulating glycogen rea#down,

gluconeogenesis, lipolysis, and #etogenesis. Hi#ewise, postprandial

insulin replacement should e appropriate for the carohydrate inta#e

and promote normal glucose utili@ation and storage.

Insulin preparations:

Short acting insulin: Regular insulin.

Intermediate acting: D&9.

Hong acting: Glargin, ultralente.

*ominations: i'ed


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care of individuals with type ) must also include attention to the

treatment of conditions associated with type ) !oesity,

hypertension, dyslipidemia, cardiovascular disease" and detection E

management of )-related complications. )-specific complications

may e present in up to 5 to $56 of individuals with newly diagnosed

type ).

?egin with diet therapy for one month, if glycemic control is not

reached drug therapy is to e started.

3ral glucose lowering drugs are to e used in type diaetes

only, they are ineffective in type 1 ).

3ral drugs:

%hose increasing insulin secretion: Sulphonylurea,

glyenclamide !daonil", glipi@ide !diamicron", glimepride

!amaryl". Side effects: hypoglycemia, weight gain.

?iguanides: Increase glucose utili@ation, decraese hepatic

glucose production, promote weight loss !metformine U

glucophage".

Alpha glucosidase inhiitors: &revent glucose asorption

!acarose U glucoay".

%hia@olidinediones: Dew group reduce insulin resistance,

increase glucose utili@ation !rosiglita@one U avandia". Side

effects: weight gain.

Insulin therapy in type ):

Insulin should e considered as the initial therapy in type ),

particularly in lean individuals or those with severe weight loss,

in individuals with underlying renal or hepatic disease that

precludes oral glucose-lowering agents, or in individuals who

are hospitali@ed or acutely ill.

&regnancy, patients with transplanted #idney.


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Insulin therapy is ultimately re;uired y a sustantial numer of

individuals with type ) ecause of the progressive nature of

the disorder and the relative insulin deficiency that develops in

patients with long-standing diaetes.

%reatment is started as single dose of S.* intermediate acting

insulin at edtimeB it can e comined with oral drugs.

Dew treatment:

&ancreatic transplantation.

&ancreatic islet cell transplantation.

*omplications of )

1- Acute complications:

a- )iaetic #etoacidosis.

- Don-#etotic hyperosmolar state.

c- 9ypoglycemia.

)IA?2%I* L2%3A*I)3SIS !)LA"

It is seen mainly in type 1 ) more than type ).

It is potentially associated with serious complications if not treated

promptly.

Symptoms:

Dausea and vomiting are often present, thirst and polyuria due to

hyperglycemia and glucosuria leading to dehydration, tachycardia and

hypotension, adominal pain, altered mental state, rapid acidotic

reathing.

&hysical signs:


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It is most commonly seen in elderly individuals with type ). Its most

prominent features include polyuriaB orthostatic hypotensionB and a

variety of neurologic symptoms that include altered mental status,

lethargy, sei@ure, and possily coma.

%reatment:

%he patient with DL9S is usually older, more li#ely to have mental

status changes, and thus more li#ely to have a life-threatening

precipitating event with accompanying complications. 2ven with proper

treatment, DL9S has a higher mortality than )LA up to $56.

9ypotonic saline infusion !5.$6 saline" should e used. After

hemodynamic staility is reached, correct the free water deficit using

hypotonic fluids !5.$6 saline initially then $6 de'trose in water". %he

calculated free water deficit !which averages J to 15 H" should e

reversed over the ne't 1 to days. &otassium repletion is usually

necessary.

+luid therapy lowers glucose initiallyB insulin therapy is less re;uired

than )LA, insulin $ to 15 units first followed y intravenous constant

infusion rate !/ to < unitsh".

9ypoglycemia:

%he most serious complication of diaetes mellitus therapy.

Symptoms:?ehavioral changes, confusion, fatigue, sei@ure, loss of consciousness,

and, if hypoglycemia is severe and prolonged, death.

9ypoglycemia-induced autonomic responses include palpitations,

tremor, and an'iety as well as cholinergic symptoms such as sweating,

hunger, and paresthesia.

%reatment:

3ral treatment with glucose talets or glucose-containing fluids, candy,

or food. A reasonale initial dose is 5 g of glucose. &arenteral therapy


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is necessary. Intravenous glucose !$ g" should e given using a $56

solution followed y a constant infusion of $ or 156 de'trose.

*9R3DI* *3&HI*A%I3DS of )

>ascular complications:

1- icrovascular:

a- 2ye complications: retinopathy, cataract, glaucoma.

- Deuropathy: Sensory, motor, autonomic.

c- Dephropathy.

- acrovascular:

a- *oronary artery disease.

- &eripheral vascular disease.

c- *ererovascular disease.

Don-vascular complications:

a- Gastrointestinal !gastroparesis, diarrhea".

- Genitourinary !Se'ual dysfunction".

c- )ermatologic.

echanisms of chronic complications:

%hese complications result from chronic hyperglycemia in type 1) and

type ).

%here are theories e'plaining the possiility of complications to e due

to either:

&roduction of intracellular sustances that accelerate

atherosclerosis, promote glomerular dysfunction, reduce nitric

o'ide synthesis, induce endothelial dysfunction, and alter

e'tracellular matri' composition and structure.

9yperglycemia increases glucose metaolism via a pathway that

produces sustances !Soritol E diacylglycerol" causing cellular

dysfunction, and promote complications.


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D.?: Studies showed that improvement of glycemic control reduced nonproliferative

and proliferative retinopathy !


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R2DAH *3&HI*A%I3DS 3+ )IA?2%2S 2HHI%S"

)iaetic nephropathy is the leading cause of end stage renal failure

in the nited States. &roteinuria in individuals with ) is

associated with mar#edly reduced survival and increased ris# of

cardiovascular disease. Individuals with diaetic nephropathy

almost always have diaetic retinopathy also.

%he cause is due to chronic hyperglycemia that causes

hemodynamic alterations in the renal microcirculation !glomerular

hyperfiltration, increased glomerular capillary pressure", and

structural changes in the glomerulus, Smo#ing accelerates thedecline in renal function.

$ to 15 years of type 1 ) 56 of individuals egin to e'crete small

amounts of alumin in the urine: microaluminuria which is defined

as /5 to /55 mgd in a -h collection. %he appearance of

microaluminuria !incipient nephropathy" in type 1 ) is a very

important predictor of progression to overt proteinuria !V/55 mgd",which once present a steady decline in G+R !Glomerular filtration

rate" occur, and $56 of individuals reach 2SR) in < to 15 years.

D.?: &atients with ) are predisposed to radiocontrast-induced nephroto'icity.

%reatment of diaetic nephropathy:

&revention is the optimal therapy, strict glycemic control, control of

lood pressure, and A*2I treatment which slows the progression to

overt nephropathy if given in the microaluminuria stage.

If the patient develops renal failure, dialysis then renal transplantation is

considered.

Deuropathy:


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)iaetic neuropathy occurs in appro'imately $56 of individuals with

long-standing type 1 and type ), the development of neuropathy

correlates with the duration of diaetes and glycemic control.

&olyneuropathy:

%he most common form of diaetic neuropathy is distal symmetrical

polyneuropathy.presents with distal sensory loss. 9yperesthesia,

parathesia, and pain may also occur.

&hysical e'amination reveals sensory loss, loss of an#le refle'es, and

anormal position sense. &arethesia is characteristically perceived as a

sensation of numness, tingling, sharpness, or urning that egins in

the feet and spreads pro'imally.

Deuropathic pain develops in some of these individuals, occasionally

preceded y improvement in their glycemic control.

&ain typically involves the lower e'tremities, is usually present at rest,

and worsens at night.

ononeuropathy, polyradiculopathy, and autonomic neuropathy:

ononeuropathy is pain and motor wea#ness in the distriution of a

single nerve, most commonly cranial nerves, the third cranial nerve is

the most commonly affected and starts y diplopia. &hysical

e'amination reveals ptosis and opthalmoplegia with normal papillary

constriction to light.

)iaetic polyradiculopathy:

Is a syndrome characteri@ed y severe disaling pain in the distriution

of one or more nerve roots. It may e accompanied y motor wea#ness.

Intercostal or truncal radiculopathy causes pain over the thora' or

adomen. Involvement of the lumar ple'us or femoral nerve may cause

pain in the thigh or hip and may e associated with muscle wea#ness in

the hip fle'ors or e'tensors. It is a self limiting condition within a year.


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Autonomic neuropathies:

Affection of the autonomic nervous system, symptoms vary according

to the system affected.

*ardiovascular system causes resting tachycardia and orthostatic

hypotension. Reports of sudden death have also een attriuted to

autonomic neuropathy.

Gastroparesis and ladder-emptying anormalities are also li#ely

related to the autonomic neuropathy seen in ).

9yperhidrosis of the upper e'tremities and anhidrosis of the lower

e'tremities result from sympathetic nervous system dysfunction!

%he patient may not feel symptoms of hypoglycemia.

%reatment of diaetic neuropathy:

%reatment is not satisfactory, control of lood sugar may improve a little

the nerve function ut not the symptoms.

Avoidance of neuroto'ins !alcohol", supplementation with vitamins for

possile deficiencies !?1, ?, folate".

Symptomatic treatment with analgesics !DSAI)S", antidepressants,

gaapentin, and carama@epine.

Gastrointestinal complications:

Hongstanding ) may affect the motility and function of the gut,

through autonomic neuropathy.Gastroparesis may present with

symptoms of anore'ia, nausea, vomiting, early satiety, and adominal

distension. Docturnal diarrhea, alternating with constipation, is a

common feature of )-related GI autonomic neuropathy.

Genitourinary complications:

*ystopathy egin with an inaility to sense a full ladder and a failure to

void completely. As ladder contractility worsens, ladder capacity and

the postvoid residual increase, leading to symptoms of urinary


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hesitancy, decreased voiding fre;uency, incontinence, and recurrent

urinary tract infections.

2rectile dysfunction and female se'ual dysfunction !reduced se'ual

desire, dyspareunia, reduced vaginal lurication".

2rectile dysfunction and retrograde eaculation are very common in )

and may e one of the earliest signs of diaetic neuropathy.

%reatment:

Glycemic control, and symptomatic treatment for nausea and vomiting

as metoclopramid, and domperidone. Symptomatic treatment for

impotence, and cystopathy.

Hower lims complications:

)iaetes is the leading cause of nontraumatic lower e'tremity

amputation in the nited States. +oot ulcers and infections are also a

maor source of moridity in individuals with ).

any factors are involved in the pathogenesis of these complications,

neuropathy interferes with normal protective mechanisms and allows

the patient to sustain repeated trauma to the foot, peripheral vascular

disease leading to poor wound healing.

Autonomic neuropathy results in anhidrosis promoting drying of the

s#in, fissure formation, and hence s#in ulceration.

Ris# factors for foot ulcers or amputation include: male se', diaetes

V15 years= duration, peripheral neuropathy, anormal structure of foot

!ony anormalities, callus, and thic#ened nails", peripheral vascular

disease, smo#ing, and history of previous ulcer or amputation.

%reatment:

%he optimal therapy for foot ulcers and amputations is prevention, y

patient education especially high ris# patients:

1. *areful selection of footwear.


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. )aily inspection of the feet to detect early signs of poor-fitting footwear or minor trauma.

/. )aily foot hygiene to #eep the s#in clean and moist.

. Avoidance of self-treatment of foot anormalities and high-ris# ehavior !e.g. wal#ing arefoot".

$. *onsultation if an anormality arises.

*orrect other ris# factors for vascular disease !smo#ing, dyslipidemia,

and hypertension" and improve glycemic control.

*areful surgical and medical therapy for patients with infected foot

ulceration is mandatory.

Hiaility to infection in ):

&atients with ) show greater fre;uency and severity of infection,

which may e due to anormalities in cell-mediated immunity and

phagocyte function associated with hyperglycemia, as well as

diminished vasculari@ation secondary to long-standing diaetes.

9yperglycemia li#ely aids the coloni@ation and growth of a variety of

organisms !Candidaand other fungal species".

&neumonia, urinary tract infections, and s#in and soft tissue infections

are all more common in the diaetic population.

Gram-negative organisms, + aureus, and ycoacterium tuerculosis

are more fre;uent pathogens.

)iaetic s#in complications:

1. %he most common s#in complication is protracted wound healing,

and s#in ulceration.

. )iaetic dermopathy, sometimes termed pigmented pretiial papules,

or (diaetic s#in spots,( egins as an erythematous area then ends

in a circular hyperpigmentation. Sometimes pretiial ullae. %his

lesion results from minor mechanical trauma in the pretiial region

and are more common in elderly men with ).


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/. Decroiosis lipoidica diaeticorum, a rare lesion affects young

women with type 1 ), it starts as erythematous pla;ue or papules

that gradually enlarge, dar#en, and develop irregular margins, with

atrophic centers and central ulceration.

. Acanthosis nigricans !sometimes a feature of severe insulin

resistance", hyperpigmented velvety pla;ues seen on the nec# or

e'tensor surfaces.

$. 3ther manifestations as lipoatrophy occuring at insulin inection

sites, scleredema !areas of s#in thic#ening on the ac# or nec# at the

site of previous superficial infections" are more common in the

diaetic population. and granuloma annulare !erythematous pla;ues

on the e'tremities or trun#".

Anemia

)efinition:

A pathological deficiency in the o'ygen-carrying component of the

lood, measured in unit volume concentrations of hemogloin, red

lood cell volume, or red lood cell numer.

3r anemia is a condition in which there is reduction of of R?*s count

and or hemogloin content due to either lood loss, decreased

production, or increased destruction of R?*s.

Regulation of R?*s production:

Red cell production occur in the one marrow, erythropoeitin hormone

is released from the #idney and regulates day to day production of

R?*s. 2rythropoeitinsecretion occur if there is impaired 3delivery to

the #idney e.g: decreased red cell mass !anemia", impaired 3loading

of the hemogloin molecule !hypo'emia", or, rarely, impaired lood flow

to the #idney !renal artery stenosis".


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Dormal life span of R?*s is 15 days, so 115 of the total cell mass

must e replaced daily, these young cells are called reticulocytes , they

represent one marrow activity.

*lassification of anemias:

1. Anemia due to lood loss: Acute or chronic.

. Anemia due to decreased red cell production.

a- 9ypochromic microcytic: ! reduced *> and *9"

i- Iron deficiency anemia.

ii- Anemia of chronic disease.

- Dormochromic normocytic:! Dormal *> and *9"i- 9ypoproliferative ! Renal disease, endocrine disease".

ii- Aplastic anemia.

c- egaloplastic anemia: ! Incraesed *> ":

i- Anemia due to ?1, folic acid, or copper

deficiency.

/- Anemia due to e'cessive red cell destruction: ! 9emolytic anemia"

*linical picture of anemia:

1. ild anemia may e discovered accidentally during routine

laoratory tests, it may not give rise to symptoms. Symptoms

depend upon the severity and duration of anemia.

. Symptoms associated with moderate or severe anemia include

fatigue, wea#ness, loss of energy, reathlessness, di@@iness,

headache, spots on vision, irritaility, amenorrhea and tachycardia

!particularly with physical e'ertion". 9owever, ecause of the

intrinsic compensatory mechanisms !changes in the cardiac output

and regional lood flow", the gradual onset of anemia particularly in

young patients may not e associated with signs or symptoms until

the anemia is severe: Whemogloin < to 4 gdHX.

/. Symptoms and signs associated with specific types of anemia:

a- Iron deficiency anemia: Associated with smooth tongue, spoon

nails, low serum iron, microcytic hypochromic anemia.


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- ?1 deficiency: GI% involvement, *DS involvement, low ?1

level, megalolastic anemia.

c- Aplastic anemia: &atient may give history of e'posure to

to'ines, hypoplastic one marrow.

d- 9emolytic anemia: Acute hemolysis is associated with

increased indirect iliruin, e'cess uroilinogen in urine and stools,

increased reticulocytic count, hyperplastic one marrow.

Haoratory evaluation:

%o diagnose anemia, routine investigations include:

1. *?*U complete lood picture including:

9emogloin: !normal 9: 1/-14 gmdl for males, and 1-1

gmdl for females".

R?*s count: ,1$5 555 - , J55 555 mmY.

9ematocrite value: &ac#ed cell volume:

- ales: -$6.

- +emales: /


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9ematocrite /


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%reatment of Iron deficiency anemia:

1. 3ral iron therapy:

+errous sulphate.

+errous fumarate.

D.?: Iron preparations may cause gastric upsets, vomiting,

constipation, and adominal pain.

. &arenteral iron therapy: Is used for patients who cannot tolerate

oral iron, or need more iron supply.

/. Red cell transfusion: pac#ed R?*s transfusion is used in patients

with severe anemia, unstale cardiovascular system, cells are

given as iron stores to e reused.

Aplastic anemia

Aplastic anemia is pancytopenia with one marrow hypocellularity. A

common occurrence of marrow hypocellularity after intensive cytoto'ic

chemotherapy for cancer.

2tiology:

Radiation:Duclear accidents.

*hemicals:?en@ene causesaplastic anemia, acute leu#emia, and

lood and marrow anormalities.

)rugs: *ytoto'ic drugs, chloramphenicol, insecticides, DSAI)S,

antiiotics, sulphonamides.

Infections:9epatitis is the most common preceding infection,

patients are usually young men who have recovered from a mild

out of liver inflammation 1 to months earlierB the suse;uent

pancytopenia is very severe.

*ongenital or inherited disease.

*linical features:


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?leeding is the most common early symptomB a complaint of

days to wee#s of easy ruising, oo@ing from the gums, nose

leeds, heavy menstrual flow, and sometimes petechiae will have

een noticed. Cith thromocytopenia, massive hemorrhage is unusual, ut

small amounts of leeding in the central nervous system can

result in catastrophic intracranial or retinal hemorrhage.

Symptoms of anemia are also fre;uent, including lassitude,

wea#ness, shortness of reath, and a pounding sensation in the

ears.

Infection is an unusual first symptom in aplastic anemia !unli#e in

agranulocytosis, where pharyngitis, anorectal infection, or fran#

sepsis occur early".

&atients often feel and loo# remar#aly well despite drastically

reduced lood counts.

Systemic complaints and weight loss should point to other

etiologies of pancytopenia.

9istory of drug use, chemical e'posure, and preceding viral

illnesses is usually found.

&hysical 2'amination: &etechiae and ecchymoses are often

present, and retinal hemorrhages may e present. &allor of the

s#in and mucous memranes is common.

Haoratory study:

&ancytopenia in peripheral lood.

9ypocellular one marrow.

%reatment:

)iscontinue drugs that may e responsile for one marrow

depression.

?one marrow transplantation: the est therapy in young adults.

Immunosuppressive drugs may induce recovery, may ecomined with transplantation.


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Supportive treatment: %reatment of infection, R?*s and platelet

transfusion to maintain their count.

9emolytic anemia

)efinition:

Dormal life span of R?*s is 15 days, when they age they are destroyed

y the Reticuloendothelial system mainly in the spleen, the main feature

of hemolysis is shortened R?*s life span, hemolytic anemia results

when one marrow cannot compensate for R?*s destruction.

*auses:a- 9emolysis due to an e'trinsic cause:

i- 9ypersplenism.

ii- Autoimmune hemolytic anemia.

- 9emolysis due to a defect in the R?*s:

i- emrane defect !&orphyria"

ii- 2n@yme defect ! G&) deficiency".

iii- 9emogloin defect: !%halassemia, sic#le cell anemia"

*linical and laoratory features:

Acute hemolysis !hemolytic crisis" is uncommon, may e

accompanied y chills, fever, ac# pain, and adominal pain,

shoc#.

Increased R?*s destruction is associated with aundice !indirect

type", and splenomegaly.

Increased reticulocytic count ! due to active one marrow".

9yperactive one marrow.

7aundice is associated with dar# stools!uroilinogen", and normal

colored urine.

&igment stones may form in the gall ladder in chronic hemolysis.

%reatment according to the cause of hemolysis.


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&urpura E coagulation defects

&urpura:Small !/ mm" red lesions in the s#in, due to

e'travasation of red lood cells into the dermis, the lesions do not

lanch with pressure. It may e palpale !raised over the surface",

or non-palpale.

&etechiae:Smaller lesions ! mm ".

*auses of purpura:

1. &rimary s#in disease: trauma, solar, steroids.

. Systemic disease:

Don-palpale:

&latelet defect: %hromocytopenia, anormal

platelet function.

*lotting factor defect.

>ascular fragility: Amyloidosis, scurvy.

%hromi: %hromotic thromocytopenic purpura

!%%&", )I*.

2molic: +at emolism.

&alpale:

>asculitis: &olyarteritis nodosa, allergic vasculitis

!9enoch-Schonlein purpura".

2molic: Acute meningococcemia.

%hromocytopenia:


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Reduction of the platelet numer, which may e due to failure of

production as in cases of marrow aplasia, firosis, or infiltration with

malignant cells, increased destruction as in idiopathic

thromocytopenic purpura !I%&", or increased splenic se;uestration,

when the spleen enlarges, the fraction of se;uestered platelets

increases, lowering the platelet count. %he most common cause of

splenomegaly is portal hypertension secondary to liver disease.

)rug induced thromocytopenia

)rugs causing reduction of platelets are antiiotics li#e sulpha drugs,

penicillin, cephalosporins, thia@ide diuretics, heparin or cytoto'ic drugs.

%he mechanism is either depression of mega#aryocyte production !e.g

cytoto'ic drugs", or through an immune response !most drugs".

ost patients recover after drug withdrawal


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%hese patients have an autoimmune disorder with antiodies directed

against target antigens in the platelets.

?one marrow e'amination shows aundant mega#aryocytes.

%reatment: *orticosteroids, splenectomy.

)rug induced platelet dysfunction:

DSAI)s, antihistaminics, antidepressants, inhiit platelet aggregation,

causing prolongation of leeding time.

So aspirin is used as a prophylactic treatment of ischemic heart disease

to prevent platelet aggregation and thromus formation.

9enoch-Schonlein purpura : !Anaphylactoid purpura"

It is a systemic vasculitis syndrome that is characteri@ed y palpale

purpura !most commonly distriuted over the uttoc#s and lower

e'tremities", arthralgias, gastrointestinal signs and symptoms, and

glomerulonephritis. It is a small vessel vasculitis.

2tiology:

%he disease is usually seen in childrenB most patients range in age from

to < yearsB however, the disease may also e seen in infants and

adults, it is an immune comple' disease triggered y upper respiratory

tract infection, drugs, or immunisations.

Symptoms:

%he typical palpale purpura is seen in virtually all patientsB most

patients develop polyarthralgias in the asence of fran# arthritis.

Gastrointestinal involvement, which is seen in almost


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to proteinuria and microscopic hematuria, renal failure is the most

common cause of death which rarely occurs in those patients.

%reatment:ost patients recover without treatment, corticosteroids may e

needed.

*oagulation defects

Inherited plasma coagulation disorders are due to defects in

single coagulation proteins, with the two F-lin#ed disorders,

factors 4 and J deficiency.

Ac;uired coagulation disorders:

- disseminated intravascular coagulation !)I*".

- %he hemorrhagic diathesis of liver disease.

- >itamin L deficiency and complications of anticoagulants.

9ereditary coagulation disorders

%he hemophilias:

?leeding disorder due to inherited deficiencies of coagulation factors,

most commonly is factor 4 or factor J.9emophilia is inherited as '- lin#ed trait, male patients only develop the

disease, while females carriers transmitt the anormal gene.

Symptoms:

Start in early childhood, persist through life, leeding develop from

trivial inury causing pathognomonic leeding manifestations

!9emarthrosis, hematomas, hematuria".


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)iagnosis: )efective factor 4 or J, prolonged &%%.

%reatment:

+actor 4 transfusion.

Ac;uired coagulation disorders

1- )eficiency of the vitamine L dependent coagulation

factors:

%here is comined dficiency of factors


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- )isseminated intravascular coagulopathy !)I*":

A coagulation disorder resulting from widespread activation of the

clotting mechanism.

2tiology:Activation of the clotting mechanism y tissue or acterial products

introduced in the lood stream, results in e'tensive firin deposition on

the arterial surfaces, depleting firinogen, prothromin, factor $ and

General Medicine ,Dentistry Second Term

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