1445 Simon Board Simulation in Nephrology and Hypertension

8/10/2019 1445 Simon Board Simulation in Nephrology and Hypertension

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Nephrology Board Simulation

James F. Simon, MDNephrology Fellowship Program Director

Department of Nephrology and HypertensionCleveland Clinic

Objectives

The practice taking the Internal Medicine Board

exam using board-related Nephrology questions

To review key educational points in determining

the correct responses to board-relatedNephrology questions


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Case 1

A 26-year old male presents with leg edema forone week

He has been using ibuprofen 800 mg 3x/day for

one month for a shoulder injury

Exam is significant for a blood pressure of 130/90

and 3+ lower extremity edema

Urinalysis: 4+ protein, no blood

24-hour urine protein: 10.8 grams, no hematuria

Serum creatinine: 0.9 mg/dL (eGFR >60cc/min)

Question 1: The most likely disordercausing this clinical picture is:

A. Human Immunodeficiency Virus (HIV)

nephropathy

B. Focal segmental glomerulosclerosis

C. Acute tubular necrosis

D. Minimal change disease


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Answer 1. D

Minimal Change Disease Nephrotic syndrome without hematuria

Preserved renal function most commonly

15% of adults may present with ATN due to volume

depletion

Steroids first-line therapy

Answer 1. D (Minimal Change Disease)

5 ways glomerular disease can present:

1. Asymptomatic hematuria

2. Acute nephritis

3. Rapidly progressive glomerulonephritis4. Chronic nephritis

5. Nephrotic syndrome:>3gm proteinuria,

edema, low albumin, hyperlipidemia


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Secondary causes of minimal change

disease

**NSAIDs Other medications include Gold, Lithium

Blood tumors:Hodgkins, leukemias

Insect bites, other antigenic stimuli

Treat underlying illness or remove offendingagents


Treatment of Primary Minimal Change

1. High dose steroids8-12 weeks

2. Oral cyclophosphamide

3. Oral cyclosporine

Responses to Treatment

1. Steroid responsive

2. Steroid dependent

3. Steroid resistant


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Answer 1. Other Options

A. HIV Associated Nephropathy (HIVAN)

Nephrotic syndrome with decreased kidney

function

Collapsing FSGS is the classic lesion

Echogenic kidneys on US

HAART mainstay of therapy Predisposition to African Americans with a

mutation in the APOL-1 genes


B. Focal Segmental Glomerulosclerosis

(FSGS)

Nephrotic syndrome, bland urinary sediment,

decreased kidney function

Most common cause of nephrotic syndrome in

adults, especially African Americans

Secondary disease

Common end-point of glomerular injury

Hyper-filtration of remnant glomeruli


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C. Acute Tubular Necrosis

Acute kidney injury manifested by

decreased kidney function

Minimal proteinuria

Ischemic, toxic most common causes

Does not present with nephrotic syndrome

Case 2

A 19 year-old male presents with tea-colored

urine, arthralgias, and a heart murmur

He lives in a dorm room at college

He had an upper respiratory infection and sore

throat 10 days agoExam reveals

Swollen and tender right wrist and left elbow

Prominent cervical/submandibular nodes

2/6 systolic ejection murmur

2+ edema


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Case 2 (cont.)

Labs Urinalysis:

SG 1.013

No glucose

pH 6.0

3+ protein

Large blood

Microscopy: 20 RBC/HPF

3 to 5 RBC casts

Blood work:

Creatinine 2.2 mg/dL

Low C3; nml C4

Glucose 51 mg/dL

Elevated rheumatoid

factor

FeNa 3.2%

Question 2: The most likely causefor this clinical scenario is:

A. Membranous glomerulonephritis

B. Wegener's granulomatosis

C. Poststreptococcal glomerulonephritisD. Acute tubular necrosis

E. Fanconi's syndrome


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Answer 2: C (Post-Streptococcal

Glomerulonephritis)5 ways glomerular disease can present:

1. Asymptomatic hematuria

2. Acute nephritis

3. Rapidly progressive glomerulonephritis

4. Chronic nephritis

5. Nephrotic syndrome: >3gm proteinuria,

edema, low albumin, hyperlipidemia


Glomerulonephritis)

Nephritic syndrome

Glomerular hematuria, tea-colored urine

Hypertension

Renal failure, often oliguric Proteinuria usually mild

Mild edema


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Glomerulonephritis)

Post-Pharyngitic Nephritis

Acute nephritis 10-14 days after a strep infection

Differentiation from IgA Nephropathy

Pharyngitis or skin infections (impetigo)

May require transient dialysis

Self-limited course, may result in permanentkidney dysfunction

If strep has been cleared, supportive treatment

Culture if active infection (and treat)

Serologies: ASO and DNAse both (or streptozyme panel)

Low C3 level during the first week

Elevated rheumatoid factor and circulating cryoglobulins

Renal failure and hematuria resolve first

Proteinuria can persist for months


Glomerulonephritis)


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Answer 2: Other Options

B. Wegeners Granulomatosis (GPA) Pulmonary-renal syndrome

ANCA-associated vasculitis

Systemic vasculitis symptoms common

Rapidly progressive crescentic GN

Life-threatening illness requiring prompt

diagnosis and treatment Steroids, cyclophosphamide or rituximab,

+/- plasmapheresis


E. Fanconi Syndrome

Not associated with renal dysfunction

Proximal renal tubular acidosis (RTA)

Hyperchloremic metabolic acidosis

Glycosuria, phosphaturia, amino acidouria

Mild proteinuria


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Case 3

A 36 year old female with recurrent kidneystones presents for further evaluation

First kidney stone approximately 15 years ago

Has passed approximately 50 stones since

Strong family history of kidney stones in her

father and brother, but no kidney failure

Type of stone is unknown She was told to restrict her calcium intake for

the past few years

Question 3: Which of the following, ifdeficient in the urine, promotes calcium

stone formation?

A. Oxalate

B. Citrate

C.Sodium

D.Proteins/amino acids

E. Uric acid


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Answer 3: B. Low Urinary Citrate

Promotes Kidney Stone Formation Urinary citrate binds urinary calcium

Non-dissociable but soluble complex

Prevents calcium from binding to oxalate or phosphate

Examples of diagnoses associated with low urinary

citrate

RTA (distal)

Medullary sponge kidney

Polycystic kidney disease

Metabolic acidosis: malabsorption, ureteral diversion


Low urine volume

Hypercalciuria

-Idiopathic

-High sodium intake

-Loop diuretics

-Hyperparathyroidism

-RTA

Hypocitraturia

-RTA

Hyperoxaluria

- Diet

- Calcium restriction

- Malabsorption

Hyperuricosuria

Urine pH

- Stone dependent

Protein loading

Risk Factors for Calcium Nephrolithiasis:


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Common management of all kidney stones

to decrease recurrence:

Increasing urine volume to over 2 L per day

2000mg daily sodium restriction

DO NOT restrict calcium intake

Limit high animal fat diets

Question 4: Renal manifestations of HIV

infection include which of the following?

A. Hyponatremia

B. Tubuloreticular inclusions

C. Focal segmental glomerular sclerosis

D. Acute tubular necrosis

E. All the above


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Answer 4: E (all the above)

A. Hyponatremia

Seen in 60% of HIV patients during their

disease

Volume depletion with up-regulation of AVP

SIADH with pulmonary and intracranial disease

Toxoplasmosis

Tuberculosis Pneumocystis


B. Tubuloreticular Inclusions

Associated with IFN up-regulation

Can also be seen in lupus nephritis and after

treatment of HCV with IFN

Seen on biopsy

C. Focal Segmental Glomerulosclerosis

Previously discussed


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D. Acute Tubular Necrosis

Acute renal failure in HIV:

ATN: medications, hypovolemia, shock

AIN: medications, infection

HUS/TTP

Crystal-induced:

acyclovir, indinavir,sulfa drugs

Indinavir Crystals

Case 5

A 65 year-old male with BPH presents for follow-up 5

days into treatment of a urinary tract infection with

trimethoprim-sulfamethoxazole. His symptoms have

resolved. Temperature 37.5 C; the remainder of the

physical exam is normal. Lab work obtained shows:

2 weeks prior Current

BUN 12 mg/dl 12 mg/dl

Creatinine 1.4 mg/dl 2.0 mg/dl


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Urinalysis:

S.G. 1.010

Heme: neg.

Protein: neg.

Leukocyte esterase: negative

No casts or cells

Case 5 (Contd)

Question 5: In the above patient, themost likely reason for the creatinine

increase to 2.0 mg/dL is:

A. Acute interstitial nephritis

B. Acute pyelonephritis

C. Obstructive uropathyD. Reduced creatinine excretion

E. Acute tubular necrosis


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Answer 5: D: Reduced Creatinine

Excretion

Properties of serum creatinine excretion

Filtered by the glomerulus

Excreted by the proximal tubule

Slightly over-estimates true GFR

Certain organic cations (e.g. trimethoprim,

cimetidine) competitively inhibit creatininesecretion

Solute Clearance

Serum Concentration

Endogenous

Production

Exogenous

Addition

Glomerular

Filtration

Tubular

concentration

Urinary

excretion

Tubular

Reabsorption

Tubular

Secretion


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A. Acute Interstitial Nephritis Associated with sulfa use

Sterile pyuria, WBC casts on urine

Can be associated with fever or rash

B. Acute pyelonephritis

Infection has cleared without clinicalpyelonephritis

Not typically associated with AKI

Answer 5: Other options

C. Obstructive Uropathy

Sulfa crystals can lead to tubular obstruction,

hematuria, but not overt obstruction

Early obstruction may appear like pre-renal

azotemia, and have a low FeNa Stable BUN suggests against true AKI

E. Acute Tubular Necrosis

Stable BUN, no urinary evidence of ATN


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A 54yo Caucasian male comes to see you in

clinic

PMH:

Diabetes Mellitus Type 2Hb A1C 8.5

HypertensionHome BPs 140s/90s

HyperlipidemiaLDL 125

Stage 4 CKDeGFR 28cc/min/1.73m2

He takes aspirin 81mg daily with his other

medications

Case 6

Case 6

As part of your discussion of CKD and the risk of

progressing to ESRD, you discuss the elevated

cardiovascular risk associated with CKD

Which of the following changes has been shownto decrease cardiovascular risk in this patient?


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(A) Lowering the glycated hemoglobin level to lessthan 6%, compared with 77.9%

(B) Controlling the systolic blood pressure to less

than 120 mmHg, compared with less than 140

mmHg

(C) Administering aspirin 325 mg daily, compared

with 81 mg daily(D) Administering simvastatin plus ezetimibe,

compared with placebo

Question 6

First prospective trial to demonstrate CV

risk reduction with lipid lowering agents in

patients with CKD 4

9270 patients, >40 years old with SCr

>1.7mg/dL in men, >1.5mg/dL in women Mean eGFR 26.6cc/min

Dialysis and non-dialysis dependent CKD

Ezetimide/simvasatin vs. placebo

Primary prevention

SHARP Trial

Baigent, Lancet, 377, 2011


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Primary outcome: atherosclerotic events

Nonfatal MI, coronary death, non-hemorrhagic stroke,

arterial revascularization

Median follow-up 4.9 years

Outcomes favored treatment arm

11.3% vs. 13.4% (RR 0.83, 95% CI 0.74-0.94)

Subgroup analysis: (not power for subgroups) No benefit in ESRD: RR 0.9 (0.75-1.08)

Benefit in non-dialysis CKD: RR 0.78 (0.67-0.91)

SHARP Trial

Baigent, Lancet, 377, 2011

(Allpost-hoc)

Primary Prevention:

CARDS: atorvastatin, DM and CKD

MEGA: pravastatin, Japanese

JUPITER: rosuvastatin, high CRP

AFCAPS: lovastatin

Secondary Prevention:

ALLIANCE: atorvastatin

4S: simvastatin

Trials Showing Benefit of

Statins in CKD 3


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AURORA: rosuvastatin

3.8-year follow-up

4D: atorvastatin

4-year follow-up

SHARP

Despite significant LDL reduction

Statins of No Benefit in ESRD

Statin therapy demonstrated benefits:

Primary prevention in CKD 3

Secondary prevention in CKD 3

No proven benefit (yet) in CKD 4 Combination simvastatin/ezetimide

Primary prevention in CKD 4

No benefits in ESRD

Summary of Lipid Therapy in CKD


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Other Options ACCORD Trial

CV risk reduction in diabetes mellitus

No benefit of intensive BP control

SBP


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Medications: clonidine 0.1mg bid, atenolol 50mgdaily, HCTZ 25mg daily, lisinopril 20mg daily (new 1

year ago)

Labs:

Plasma renin activity 6 mg/L/hr; Aldosterone 10 ng/dL

Na+ 136; K+ 3.3; CO2 27; BUN 45; Creatinine 1.6Urinary protein:creatinine ratio 0.6gm/gm

Renal artery duplex: 60-99% bilateral RAS

Case 7 (Contd)

Question 7: If renal artery stenosis is found onangiography, which indication for angioplasty

and stenting does this patient have?

A. Resistant hypertension

B. Preservation of renal function

C. Worsening renal function on an ACE

inhibitor

D. Hypokalemia

E. Congestive heart failure


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Answer 7:

E. Congestive Heart FailureUnderstanding the ACC/AHA guidelines for

revascularization of renal artery stenosis

Accelerated, resistant or malignant

hypertension

Progressive renal dysfunction in the setting of

bilateral RAS or RAS to a solitary functioningkidney

Congestive heart failure or unstable angina

Answer 7:E. Congestive Heart Failure

Retrospective studies consistently support the

link between CHF and RAS

Flash pulmonary edema or recurrent CHF

exacerbations with RAS occur in bilateral RAS or

RAS to solitary functioning kidney

Intervention can improve symptoms, BP control and

kidney function

Prospective studies suggest improvement in

chronic CHF with bilateral RAS


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Often present with acute pulmonary edema and

hypertension

Catecholamine-driven process that cycles

BP may spike and drop multiple times during an

admission

Pulmonary edema will trend with BP spikes

Answer 7:E. Congestive Heart Failure

Answer 7: Other Answers

A. Resistant Hypertension

Refractory to 3 maximally dosed anti-hypertensive

medications, including a diuretic

Make sure of three things:

The drugs are maximally dosed (amlodipine 2.5mg/day) The dosing intervals are appropriate (clonidine bid or

atenolol daily)

The drugs are the most efficacious in their class (atenolol,

+/- HCTZ)

Does not meet definition of resistant HTN


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Answer 7: Other Answers

D. Hypokalemia

While hypokalemia might suggest an up-regulated

renin/angiotensin/aldosterone system, it certainly is

not an indication alone

Thiazide therapy can explain this

Safian, NEJM 344(6):431, 2001

Presentations of RAS

HTN

Renal Failure

Both

Neither

CHF


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Renovascular Hypertension

Onset in women 55 years old (AS)

Newly worsening hypertension

Resistanthypertension

Abdominal bruitsnon-specific in elderly

patients

Secondary Hypertension:

Obstructive sleep apnea

Hyper/Hypo-Thyroidism

Contraceptives, Coarcation of aorta, Cushings

Renal artery stenosis, Renal diseaseAldosteronism (primary and other)

Pheochromocytoma


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Case 8:

A 55-year-old male with a history of smallcell lung cancer is admitted to the hospital

with weakness and confusion for the past 48

hours. He became minimally arousable this

morning

BP 126/70, weight 65kg

He is arousable, not orientedOral mucosa are moist

Lungs are clear, no edema

Case 8, contd:

Serum

Sodium 118 mmol/L

Potassium 4.0 mmol/L

Cl 84 mmol/L

CO2 22 mmol/LBUN 9 mg/L

Creatinine 0.9 mg/dL

Glucose 90 mg/dL

Uric acid 2.5 mg/dL

Urine

Osmolality 450 mOsm/L

Sodium 50 mmol/L


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Question 8: Which of the following

treatments will NOT lead to a rise in

serum sodium in this patient?

A. Effective treatment of the malignancy if

available

B. Free water restriction

C. Vasopressin antagonists

D. Isotonic saline

E. Furosemide

Answer 8: D. Isotonic saline

Syndrome of Inappropriate ADH Secretion

(SIADH)

Known small cell lung cancer

Hyponatremia

High urinary sodium and osmolality Low serum uric acid level


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Urine Parameters and

Hyponatremia

Intravascular

Vol. Depletion SIADH Polydipsia

UNa

UOsm

Renal Handling of Water

Osmolality

1200

Osmolality

50

Na

K

2Cl

AQ2

H2O

Osmolar

load

Water load

Urine

Osmolality

AVP


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Renal Handling of a Water Load

Assume 600mOsmo dietary intake

Minimal urinary osmolality of 50 mOsm/L

Maximum urinary osmolality of 1200 mOsm/L

What is the minimum and maximum amount of

water you can drink in a day and still handle the

water load solely through urination?

0.5L12L



Minimal urinary osmolality of 100 mOsmo/L

Maximum urinary osmolality of 800 mOsmo/L

(elderly female tea and toaster)

What is the minimum and maximum amount of

water you can drink in a day and still handle the

water load solely through urination?

0.25L2L (8 cups of tea per day)


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Any water intake beyond the maximum amount

for a given minimum urinary osmolality must be

retained as free water

Leads directly to hyponatremia

Renal Handling of a Water Load:SIADH


Urinary osmolality fixed at 450mOsmo/L

What is the maximum amount of water you candrink in a day and not retain free water leading

to hyponatremia?

1.3L (600/450)


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SIADH Assume 600mOsmo dietary intake

Urinary osmolality fixed at 450mOsmo/L

What is the impact of infusing 1L normal saline

(osmolality = 308 mOsmo/L)?

0.67L urinated at 450mOsmo/L

0.33L retained free water

Sodium goes down!

Treatments for SIADH

Osmolality

1200

Osmolality

50

Na

K

2Cl

AQ2

H2O

Osmolar

load

Water load

Urine

Osmolality

AVP

Demeclocycline

Vaptans

(caution)


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Case 9

A 65yo AAM presents to your office to establish

care. He has chronic kidney disease, diabetes

mellitus, hypertension and hyperlipidemia.

H/O coronary artery disease s/p stenting to LAD

and RCA lesions 2 years ago.

Medications

Losartan 50mg twice daily -HCTZ 25mg once daily Amlodipine 5mg once daily -Pravachol 20mg at night

ASA 325mg once daily -Metformin 500mg twice daily

Glipizide 10mg daily

Case 9

BP 138/82, HR 87, BMI 32

On exam:

Lungs are clear to auscultation

Heart is regular rhythm, S4 present, 1/6 systolic

crescendo murmur at left upper sternal border

No carotid bruits

JVP 6cm

Abd: without bruits, abnormal pulsation

Extremities: diminished distal pulses, 2+ bilateral

ankle edema (which he blames on amlodipine)


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Case 9

Labs

Creatinine 2.0mg/dL, eGFR 41cc/min/1.73m2

Na 138, K 5.0, Bicarb 23, glucose 156

A1C 8.5, LDL 67, Hb 11.0

Home blood pressure readings run 130-140/75-

85

Blood sugars run 150-200 when checked in themornings

Question 9: What is the next besttherapeutic change to make?

A. Increase metformin to 1000mg twice daily

B. Add lisinopril 10mg once daily

C. Increase amlodipine to 10mg once daily

D. Add metoprolol 25mg twice daily

E. Increase pravachol to 40mg at night


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Answer 9:

D: Add metoprolol 25mg bid

Target BPs for hypertension treatment (JNC 7):

General population:


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Question 9: Other Answers

A. Increase metformin to 1000mg twice daily

Given his CKD, strong consideration should be given

to switching to another agent rather than increasing it

B. Add lisinopril 10mg once daily

ON-TARGET suggested that dual ACEi and ARB

therapy increases risk for hyperK and cardiac events

Practice not abandoned, but should be approached with

caution

High-normal K would make adding ACEi hazardous

Lancet. 2008; 372:547553

Question 9: Other Answers

C. Increase amlodipine to 10mg once daily

Patient already complains of edema on 5mg dose,

likely to be exacerbated by increase dose

Further rise in heart rate also an unwanted

consequence

E. Increase pravachol to 40mg at night

LDL goal

For CKD without CAD:


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Question 10

A 36 yo female nurse presents for furtherevaluation of fatigue and muscle cramping.

Blood pressure is normal

Examination is unremarkable

Plasma 24-hour Urine

Na+ 140 mEq/L Na+ 80 mEq/d

K+ 2.5 mEq/L K+ 170 mEq/d

Cl- 86 mEq/L Cl- 40 mEq/dCO2 28 mEq/L Ca+2 76 mg/d

Mag 1.5 mEq/L Mg+2 7 mg/d

Question 10Continued

After replenishment of her hypokalemia and

hypomagnesemia with IV solutions, her symptoms

resolve

Her only medical problem is GERD for which she

has been taking omeprazole for the past 8 months


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Question 10: Which of the following

would be the best next move?

A. Start amiloride

B. Stop the omeprazole

C. Check a diuretic screen

D. Discuss your concerns about surreptitious

vomiting

E. Start spironolactone

Hypokalemia

Etiology

1. Lack of intake

2. Cellular shifts

3. Renal wasting

Often associated with metabolic alkalosis

Hypokalemia can drive and maintain an alkalosis

24-hour urine potassium

Renal vs. non-renal


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Renal K wasting

Normo-hypotensive:

Diuretics

Diuretic mimickers

LoopBartters

ThiazideGitelmans

Hypomagnesemia

Emesis

Hypertensive:

Hyperaldosterone statesprimary / secondary

Hypomagnesemia

Etiology

Decreased intake/malabsorption

Renal wasting (cause of or association with low K)

24-hour urine magnesium vs. FeMag

GI wasting:

Short gut syndrome/malabsorption

PPIs

H+important for absorption of metals from gut

Upregulates TRPM6/7 (magnesium channels)


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Answer 10: Incorrect Options

A.Amiloride for Gitelmans syndrome Low/normal BP, low urine Ca+2, high urine Cl-,

high urine mag+2

C. Diuretic abuse Low/normal BP, high urine Cl-, high urine mag+2

D. Surreptitious vomiting

Low/normal BP, low urinary Cl-

E. Spironolactone for hyperaldostone state High BP, hypomag less not seen

Differentiating Diuretic Abuse fromBartters/Gitelmans

Both have:

High urine chloride

Upregulated renin and aldosterone

Renal wasting of K/Mag and metabolic alkalosis

History Recurring issueespecially if since childhood, think

genetic

Medical field, weight loss or other medical field

diuretic abuse

Diuretic screen will answer the question


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Differentiating Bartters from

Gitelmans Bartters:

Mimics loop diuretics

Acts at NKC2 triporter in thick ascending limb

Causes increased calcium excretion in the urine

Gitelmans:

Mimics thiazide diuretics

Acts at NaCl transporter in distal convoluted tubule Causes calcium reabsorption and low urine calcium

24 hour urine calcium collection differentiates

Hypomagnesemia-InducedRenal K+Wasting

Magnesium increases inward movement of

potassium movement through ROMK in the

collecting duct


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U

R

I

N

E

3Na+

2K+

K+

Aldo

CORTICAL COLLECTING DUCT

PRINCIPLE CELL

ENaC

BL

O

O

D

Mag+2

U

R

I

N

E

3Na+

2K+

K+

Aldo

CORTICAL COLLECTING DUCT

PRINCIPLE CELL

ENaC

B

L

O

O

D

Mag+2


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Case 11

A 28 yr-old female with 18-yr history of diabetes

mellitus is seen at 12 weeks gestation of her first

pregnancy

Enalapril 5 mg/day for HTN and diabetic nephropathy

BP 160/100. The remainder exam is normal.

Laboratory studies reveal: Hgb A1C 10%Cr 0.8 mg/dl

24 hr protein excretion 1.2 gm

Question 11: Which of the followingwould you advise?

A. Increase enalapril to 10 mg per day

B. Replace enalapril with hydrochlorothiazide 12.5mg

per day

C. Continue enalapril and add alpha-methyldopa 250mg twice a day

D. Replace enalapril with alpha-methyldopa 250 mg

twice a day

E. Continue enalapril and add amlodipine 5 mg per day


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Answer 11:

D. Replace enalapril with methyldopa Issue: Hypertension in pregnancy

(BP>140/90) Common Internal Medicine issue

Identify medications safe for use during pregnancy or

when attempting to become pregnant

Hypertension in Pregnancy

Angiotensin converting enzyme inhibitors Cross the placenta

Angiotensin II important in the regulation of placental

blood flow and normal fetal growthAssociated with fetal developmental abnormalities in

all trimesters

CV and CNS in first trimester

Renal, limb and others later


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Answer 11: Hypertension in

Pregnancy

Methyldopa

Labetolol

Long acting CCBs

nifedipine best studied

Hydralazine Thiazides considered safe if

already taking

Safe Meds

Answer 11: Hypertension in

Pregnancy

Classifications of Hypertension in Pregnancy

1. Pre-existing hypertension

Before 20 weeks gestation or lasting 12 weeks

post-partum2. Pre-eclampsia

HTN after 20 weeks, edema, proteinuria

3. Gestation hypertension

1445 Simon Board Simulation in Nephrology and Hypertension

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Transcript of 1445 Simon Board Simulation in Nephrology and Hypertension