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STEP2 COPY > Nephrology > Flashcards

Nephrology Flashcards

1
Q

What two things increase urinary protein excretion?

A

standing and physical activity

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2
Q

Urine dipstick for protein detects what specifically?

A

it only measures albumin

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3
Q

What is considered microalbuminuria?

A

30-300mg protein/day

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4
Q

What is a normal number of RBCs in urine?

A

less than 5/hpf

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5
Q

Dysmorphic RBCs found on UA are suggestive of what?

A

glomerulonephritis

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6
Q

What do each the following types of casts suggest:

  • RBC
  • WBC
  • Eosinophil
  • Hyaline
  • Muddy Brown/Granular
A
  • RBC: glomerulonephritis
  • WBC: pyelonephritis
  • Eosinophil: acute interstitial nephritis
  • Hyaline: dehydration (concentration of normal Tamm-Horsfall protein)
  • Muddy Brown/Granular: acute tubular necrosis
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7
Q

Describe the etiology, presentation, and treatment of pre-renal azotemia.

A
  • due to anything that reduces renal perfusion: hypovolemia, hypotension, renal artery stenosis, NSAID-induced afferent constriction, ACEi efferent vasodilation
  • presents with a rise in BUN/Cr greater than 20, UNa less than 20, FENa less than 1%, and UOsm > 500 since tubular function remains in tact
  • treat with volume resuscitation and avoidance of nephrotoxic agents
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8
Q

Describe the etiology, presentation, diagnosis, and treatment of post-renal azotemia..

A
  • due to anything that obstructs both kidneys: BPH, prostate adenocarcinoma, urethral stone, urethral stricture, neurogenic bladder
  • presents with enlargement of the bladder or massive diuresis after placement of a Foley
  • presents with a rise in BUN/Cr greater than 20, UNa less than 20, FENa less than 1%, and UOsm > 500 since tubular function remains in tact
  • best initial test is a renal ultrasound looking for hydronephrosis
  • treat by removing the obstruction
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9
Q

Describe the etiologies, presentation, and treatment of acute tubular necrosis.

A
  • due to ischemia or nephrotoxicity which damage the tubules: aminoglycosides, amphotericin, cisplatin, heavy metals, myoglobinuria as in crush injury, ethylene glycol and other crystals, radio contrast dye, or urate from tumor lysis syndrome
  • injury results in necrosis of tubular epithelial cells, which form brown, granular casts and diminish GFR
  • tubular dysfunction leads to elevated BUN and Cr, though the BUN/Cr is < 20, FENa > 1%, and UOsm < 300
  • clinical features include oliguria as well as hyperkalemia and acidosis due to the inability to secrete these cations
  • treatment is supportive with fluids and correction of electrolyte abnormalities; may require dialysis
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10
Q

If a patient has an AKI of unclear etiology, what is the best next step?

A
  • always get a UA first

- supplement with UNa, FENa, and UOsm

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11
Q

How should you interpret the specific gravity of urine?

A

it correlates with the UOsm:

  • 1.010 = UOsm of 100
  • 1.030 = UOsm of 300
  • 1.050 = UOsm of 500
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12
Q

Describe the pathophysiology, presentation, and prevention of contrast-induced nephropathy.

A
  • nephrotoxicity is caused by spasm of the afferent arteriole, which induces ATN
  • it presents with a very a rapid onset of injury and, oddly, urinary lab values consistent with a pre-renal azotemia (UNa < 20, FENa < 1%, UOsm > 300)
  • prevent with aggressive hydration prior to administration of contrast material
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13
Q

How does tumor lysis syndrome affect the kidneys? Describe the mechanism and prevention.

A
  • rapid lysis of tumor cells following chemotherapy may release lots of urate, which is particularly nephrotoxic
  • the result is often intra-renal azotemia (acute renal failure)
  • to prevent this, hydration and allopurinol are used prior to initiating chemotherapy
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14
Q

What do the following suggest in the setting of acute tubular necrosis:

  • rapid onset of injury
  • 5-10 day incubation period
  • hypocalcemia
A
  • rapid onset of injury: contrast-mediated
  • 5-10 day incubation period: more likely due to ahminoglycosides, amphotericin, cyclosporine, cisplatin, acyclovir, or vancomycin
  • hypocalcemia: likely ethylene glycol poisoning
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15
Q

Describe the presentation, diagnosis, and treatment of rhabdomyolysis.

A
  • presents with an elevated CPK, hyperkalemia, hyperuricemia, hyperphosphatemia, hypocalcemia, and acute tubular necrosis
  • diagnosis is based off a positive urine dipstick for blood but no RBCs present on UA
  • treat with saline and mannitol, get an ECG and monitor treat symptomatic electrolyte abnormalities
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16
Q

What are the indications for dialysis?

A 
A: acidosis < 7.1
E: electrolyte disturbances that are refractory 
I: intoxications
O: overload of fluid
U: uremic pericarditis or encephalitis
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17
Q

Describe the definition, etiology, presentation, diagnosis, and treatment of acute interstitial nephritis.

A
  • it is an idiosyncratic drug reaction causing intra-renal AKI
  • due to the 6 P’s: pee (diuretics and other sulfa drugs), pain free (NSAIDs), penicillins, PPIs, phenytoin, and rifamPin
  • presents with fever, rash, oliguria, and eosinophiluria
  • the best initial test is a UA showing BUN/Cr < 20 plus WBCs and RBCs in the urine
  • most accurate is Hansel or Wright stain for eosinophils
  • treat by removing the offending agent; try steroids if the creatinine continues to rise
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18
Q

Which drugs cause allergenic responses and how do these manifest?

A
  • due to the 6 P’s: pee (diuretics and other sulfa drugs), pain free (NSAIDs), penicillins, PPIs, phenytoin, and rifamPin
  • manifest as drug allergy, SJS, TEN, hemolysis, and acute interstitial nephritis
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19
Q

Describe the pathophysiology of analgesic nephropathy.

A
  • prostaglandins promote dilation of the afferent arteriole
  • chronic NSAID use reduces the availability of these and thus promotes constriction of the afferent arteriole
  • this decreases renal perfusion and promotes nephropathy in the form of ATN, AIN, papillary necrosis, or membraneous glomerulonephritis
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20
Q

Describe the etiology, presentation, and diagnosis of papillary necrosis.

A
  • due to sickle cell disease, diabetes, pyelonephritis, and NSAID use
  • presents with acute onset of fever, flank pain, hematuria
  • UA will show RBCs, WBCs, and necrotic kidney tissue; the most accurate test is a CT showing a bumpy counter of the renal interior where papillae were lost
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21
Q

What are the features of nephritic syndrome?

A
  • proteinuria is limited (< 3.5 g/day)
  • oliguria and azotemia
  • salt retention with periorbital edema and hypertension
  • RBC casts and dysmorphic RBCs
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22
Q

Which glomerular disease are characterized by low complement levels?

A

SLE, endocarditis, cryoglobulinemia, and post-streptococcal glomerular disease

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23
Q

Describe the presentation, diagnosis, and treatment of goodpasture disease.

A
  • also known as anti-GBM disease, it is due to antibodies against the basement membrane of alveoli and glomeruli
  • presents with hemoptysis followed by hematuria
  • the best initial test is for anti-GBM antibodies and the most accurate is kidney biopsy showing a linear pattern of IgG and C3 deposition
  • treat with plasmapheresis and steroids
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24
Q

Describe the presentation, diagnosis, and treatment of IgA nephropathy.

A
  • the most common nephropathy worldwide
  • presents with recurrent hematuria 1-2 days after a URI
  • IgA levels may be elevated but the most accurate test is kidney biopsy
  • the level of proteinuria is the best prognostic factor so treat with ACEi and steroids
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25
Q

Describe the presentation, diagnosis, and treatment of post-infectious glomerulonephritis.

A
  • presents as a nephritic syndrome arising 1-3 weeks after group A beta-hemolytic strep infection
  • diagnosis is with ASO and anti-DNase antibody titers
  • treat with antibiotics and diuretics to control fluid overload
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26
Q

Describe the pathophysiology and presentation of Alport syndrome.

A
  • an X-linked dominant type IV collagen defect
  • results in thinning and splitting of the glomerular basement membrane
  • presents with hematuria, sensory hearing loss, and ocular disturbances
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27
Q

What are the features of nephrotic syndrome?

A
  • proteinuria > 3.5g per day
  • hypoalbuminemia
  • hypogammaglobulinemia
  • hypercoagulability
  • hyperlipidemia
  • edema
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28
Q

How are nephrotic syndromes treated?

A
  • steroid with steroids then try cyclophosphamide
  • add ACEi or ARBs to control the proteinuria
  • treat edema with salt restriction and diuretics
  • treat hyperlipidemia with statins
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29
Q

Describe the pathogenesis of diabetic nephropathy.

A
  • nonenzymptic glycosylation of the vascular basement membrane results in hyaline arteriolosclerosis, reducing lumen diameter
  • efferent arteriole more affected than afferent, increasing the GFR, and this hyperfiltration injury leads to microalbuminuria
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30
Q

What are the main manifestations of ESRD?

A
  • anemia due to loss of EPO
  • hypocalcemia, hyperphosphatemia, hyperparathyroidism, and renal osteodystrophy
  • hypermagnesemia
  • platelet dysfunction
  • neutrophil dysfunction and infection
  • hypertension and accelerated atherosclerosis
  • pericarditis
  • encephalitis
  • volume overload
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31
Q

How do we treat the following manifestations of ESRD:

  • anemia
  • bleeding
  • hypocalcemia and osteodystrophy
  • hyperphosphatemia
  • hypermagenesemia
A
  • anemia: EPO and iron supplementation
  • bleeding: DDVAP when bleeding
  • hypocalcemia and osteodystrophy: vitamin D and calcium replacement
  • hyperphosphatemia: oral binders like calcium salts, sevelamer, and lanthanum
  • hypermagenesemia: dietary restriction
32
Q

What is calciphylaxis?

A

calcification of blood vessels with subsequent skin vessel clotting and necrosis which arises from hypercalcemia or hyperparathyroidism

33
Q

What is nephrogenic systemic fibrosis?

A

a proliferation of dermal fibrocytes leading to joint and skin contractors following administration of gadolinium MRI contrast material to those with GFR < 30

34
Q

Describe the pathogenesis, presentation, and treatment of hemolytic uremic syndrome.

A
  • toxins produced by E. coli O157:H7 or Shigella cause endothelial damage and formation of platelet microthrombi
  • presents as thrombocytopenia, microangiopathic anemia, and thrombocytopenia
  • can find schistocytes, elevated LDH, low haptoglobin, and prolonged bleeding time but normal PT and PTT
  • treat with plasmapheresis
35
Q

Describe the pathogenesis, presentation, and treatment fo thrombotic thrombocytopenic purpura.

A
  • auto-antibodies against ADAMTS-13 lead to release of ultra-large vWF, which causes the formation of platelet microthrombi
  • presents with a classic pentad of fever, CNS and renal abnormalities, mucocutaneous bleeding, and hemolytic anemia
  • can find schistocytes, elevated LDH, low haptoglobin, and prolonged bleeding time but normal PT and PTT
  • treat with plasmapharesis and corticosteroids
36
Q

What is different about the pathogenesis and treatment of “atypical” HUS?

A

it is caused by complement erroneously attacking RBCs rather than bacteria-producing toxin, thus it is treated with eculizumab, a C5a inhibitor

37
Q

Describe the presentation of polycystic kidney disease.

A
  • presents with polycystic kidneys, pain at the costovertebral angles, hematuria, hypertension, and ultimately kidney failure
  • associated with other connective tissue dysfunction including cerebral aneurysms, hepatic cysts, diverticulitis, and mitral valve prolapse
38
Q

How are renal cysts managed?

A
  • those that are benign (echo free with smooth thin walls and sharp demarcation) can be managed expectantly
  • those that have any complexity are potentially malignant and should be aspirated for evaluation
39
Q

What are the symptoms of hypo- and hypernatremia?

A

both cause CNS dysfunction ranging from confusion to disorientation, lethargy, seizures, and coma

40
Q

Describe the possible etiologies and workup of hypernatremia.

A

the differential includes sweating, burns, diarrhea, pneumonia, osmotic diuresis, and diabetes insipidous

  1. begin with a urine osmolarity
    - if greater than 800 (appropriately concentrated to retain free water), it is suggestive of free water loss outside of the kidneys: sweating, pneumonia, burns, diarrhea
    - if less than 800 (inappropriately low), it is suggestive of renal losses and either osmotic diuresis (glucose, uremia, mannitol) or diabetes insipidous
  2. if diabetes insipidous is suspected, the best initial test is water deprivation, which confirms the diagnosis
  3. then give ADH to differentiate central and peripheral causes
    - central can be anything that damages the HP axis
    - peripheral is likely lithium, CKD, or hypokalemia

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41
Q

Describe the pathophysiology, presentation, diagnosis, and treatment of central diabetes insipidous.

A
  • due to damage of the hypothalamus or posterior pituitary, which prevents the production of ADH
  • presents with hypernatremia and neurologic dysfunction
  • first step in diagnosis is UOsm which is inappropriately low (<800); best initial test is then a water deprivation test followed by administration of ADH to differentiate central from nephrogenic DI
  • treat with ADH replacement
42
Q

Describe the etiology, presentation, diagnosis, and treatment of nephrogenic diabetes insipidous.

A
  • due to lithium toxicity, CKD, and hypokalemia
  • presents with hyperkalemia and neurologic dysfunciton
  • first step in diagnosis is UOsm which is inappropriately low (<800); best initial test is then a water deprivation test followed by administration of ADH to differentiate central from nephrogenic DI
  • treat with correction of potassium and calcium, holding lithium, and giving HCTZ or NSAIDs
43
Q

What is the best first step in evaluating hypernatremia?

A
  • get a urine osmolarity
  • if elevated, this is an appropriate renal response and suggests extra renal free water losses: diarrhea, pneumonia, burns, sweating
  • if less than 800, this is inappropriate and suggests renal loss of free water through osmotic diuresis or DI
44
Q

What causes hypervolemic hyponatremia?

A
  • these patients are fluid overloaded but vascularly depleted which triggers a rise in ADH
  • possibly etiologies include cirrhosis, nephrotic syndrome, and CHF
45
Q

What causes hypovolemia hyponatremia?

A
  • these are the same causes of hypernatremia but after being treated with chronic free water replacement
  • this includes sweating, burns, pneumonia, diarrhea, and diuretics
  • it also includes Addison disease due to the lack of aldosterone
46
Q

How does hyperglycemia affect sodium levels?

A
  • hyperglycemia draws free water out of cells into the vascular space causing a euvolemic hyponatremia
  • corrected sodium is 1.6 mEq higher for every 100 increase in glucose above 100
47
Q

How does thyroid hormone affect serum sodium?

A

thyroid hormone is necessary for free water excretion, so hypothyroidism is a cause of euvolemic hyponatremia

48
Q

Describe the workup and etiologies of hyponatremia.

A
  1. start by assessing plasma osmolarity
    - elevated > 290 suggests hyperglycemia or mannitol
    - normal suggests pseudohyponatremia from either elevated lipids or proteins
    - decreased < 275 suggests true hyponatremia
  2. for true hyponatremia get a urine osmolarity
    - if less than 100 (maximally concentrated), it is caused by psychogenic polydipsia
    - if greater than 100, the problem is at the kidney
  3. assess volume status
    - hypervolemic: CHF, nephrotic syndrome, cirrhosis
    - euvolemic: hypothyroid, SIADH
    - hypovolemic: dehydration from GI or insensible losses, diuretic use, or Addison disease
49
Q

Describe the etiology, presentation, diagnosis, and treatment of SIADH.

A
  • most often due to CNS trauma, pulmonary infection, or small cell lung carcinoma
  • symptoms are those of hyponatremia, namely neurologic dysfunction
  • the diagnosis is suggested by a serum osmolarity < 275, a urine osmolarity > 100, and euvolemic fluid status
  • treatment is with free water restriction or demeclocycline, which inhibits the V2 intracellular cascade mediated by Gs
50
Q

How is hyponatremia treated?

A
  • for asymptomatic hyponatremia, restrict free water intake
  • for mild symptoms, give normal saline and a loop diuretic
  • for severe symptoms, give hypertonic saline and tolvaptan, an ADH antagonist
51
Q

What is the mnemonic for the etiologies of hyperkalemia?

A 
Digoxin
hyperOsmolarity
Lysis of cells
Acidosis
B-blockers
Sugars (hyperglycemia)
Succinylcholine
52
Q

Describe the etiology, presentation, diagnosis, and treatment of hyperkalemia.

A
  • caused by renal failure, low aldosterone states, and increased release from tissues (DOLABSS)
  • presents with issues of muscle contraction and cardiac conduction: weakness, ileus, and arrhythmia
  • best initial test is a ECG, which is likely to show peaked T waves, a widened QRS, and prolonged PR interval
  • for ECG changes, treat with calcium gluconate, insulin, glucose, sodium bicarbonate, and inhaled beta agonists to shift potassium into cells
  • then give loop diuretics or perform dialysis to remove potassium from the body
  • if no ECG changes are seen, give Kayexalate and loop diuretics
53
Q

Describe the etiology, presentation, diagnosis, and treatment of hypokalemia.

A
  • due to a shift into cells, loop diuretics, hyperaldosteronism, hypomagnesemia, or GI losses from vomiting and diarrhea
  • presents with issues of muscle contraction and cardiac conduction including weakness, paralysis, and loss of reflexes
  • best initial test is an ECG finding U waves and flat T waves
  • treat with oral or IV replacement, but know that rapid IV replacement can induce arrhythmia
54
Q

What is Conn syndrome?

A

another name for primary hyperaldosteronism

55
Q

What drug or hormone excess do each of the following mimic:

  • Bartter syndrome
  • Gitelman syndrome
  • Liddle syndrome
A
  • Bartter: excess furosemide
  • Gitelman: excess thiazide
  • Liddle: excess aldosterone
56
Q

What causes hypophosphatemia and what causes hyperphosphatemia?

A
  • hypo arises with feeding when more tissues are produced while hyper arises from starvation and tissue breakdown
  • as such, hypophosphatemia arises from insulin, refeeding syndrome, hyperparathyroidism, and vitamin D deficiency
57
Q

How is anion gap calculated and what is normal?

A

Na - Cl - HCO3 should be less 12

58
Q

What are two causes of non-gap metabolic acidosis? How are they differentiated?

A
  • diarrhea will have a negative urine anion gap

- RTAs will have a positive urine anion gap

59
Q

What is the urine anion gap and how is it useful?

A
  • calculated as Na minus Cl in the urine
  • because the kidneys secrete H+ as NH4Cl, the UAG will decrease as acid secretion increases
  • this helps differentiate the two causes of non-gap metabolic acidosis: diarrhea and RTA
  • in those with diarrhea and a non-gap metabolic acidosis, the kidneys try to compensate by secreting acid and Cl content of the urine rises, turning the UAG negative
  • in those with RTA, there is an inability to secrete acid so Cl content drops, turning the UAG positive
60
Q

Describe the etiology, pathophysiology, diagnosis, and treatment of a type I RTA.

A
  • due to amphotericin, autoimmune disease, or topiramate
  • a-intercalated cells are unable to secrete acid and reabsorb bicarb
  • presents with a non-gap metabolic acidosis, positive UAG, urine pH greater than 5.5, and hypokalemia
  • the most accurate test is to administer ammonium chloride; a person with type I RTA won’t be able to get ride of this acid and urine pH will remain less than 5.5
  • treat with bicarb replacement and the proximal tubule will absorb it to correct the acidosis
61
Q

Describe the etiology, pathophysiology, diagnosis, and treatment of a type II RTA.

A
  • due to myeloma, Fanconi syndrome, or acetazolamide
  • the proximal tubule is unable to reabsorb bicarbonate and at first urine pH is elevated but eventually it is all lost and urine pH drops to less than 5.5
  • presents with a non-gap metabolic acidosis, variable urine pH, and hypokalemia
  • the most accurate test is to give bicarbonate and then test urine pH which will rise
  • treat with bicarbonate replacement and thiazide diuretics
62
Q

Describe the etiology, pathophysiology, diagnosis, and treatment of type IV RTA.

A
  • due to hypoaldosteronism, usually in diabetics
  • hypoaldosteronism leads to a retention of potassium and hydrogen ions
  • presents with a non-gap metabolic acidosis, urine pH less than 5.5, and hyperkalemia
  • the most accurate test is a persistently high urine sodium despite a sodium-restricted diet
  • treat with fludrocortisone
63
Q

Compare type I, II, and IV RTAs.

A
  • I: urine pH > 5.5, hypokalemia, associated with stones
  • II: urine pH is first high and then low, hypokalemia
  • IV: urine pH is < 5.5, hyperkalemia, seen in diabetics
64
Q

What are the causes of anion-gap metabolic acidosis?

A 
Methanol
Uremia
DKA
Paraldehyde
Iron/Isoniazid
Lactate
Ethylene glycol
Salicylates
65
Q

What is unique about calcium oxalate stones?

A
  • they are the most common form of stone
  • due to excess excretion of calcium into alkaline urine
  • treat with thiazide diuretics to reduce calcium excretion
66
Q

What is unique about ammonium magnesium phosphate stones?

A
  • due to infection with urease-positive organisms like Proteus and Klebsiella
  • alkaline urine also increases the risk
  • form stag horn calculi and require surgical removal
67
Q

Kidney stones of what size are treated with the following:

  • nifedipine and tamsulosin
  • lithotripsy
  • surgical removal
A
  • nifedipine and tamsulosin: 5-10mm
  • lithotripsy: less than 2-3cm
  • surgical removal: greater than 2-3cm
68
Q

What is the treatment for stress incontinence?

A
  • start with Kegel exercises
  • add topical estrogen
  • move to surgery
69
Q

What is the treatment for urge incontinence?

A
  • start with bladder training
  • add anticholinergics
  • move to surgery
70
Q

What suggests each of the following as a cause of secondary hypertension:

  • renal artery stenosis
  • glomerulonephritis
  • coarctation of the aorta
  • pheochromocytoma
  • hyperaldosteronism
A
  • renal artery stenosis: continuous bruit heard at the flank
  • glomerulonephritis: dysmorphic RBCs on urinalysis
  • coarctation of the aorta: blood pressure differential between upper and lower extremities
  • pheochromocytoma: episodic nature
  • hyperaldosteronism: with hypokalemia
71
Q

What lifestyle modification is most effective at treating hypertension? What are others?

A
  • weight loss is most affective
  • others include sodium restriction, dietary modification, and exercise
  • smoking doesn’t stop hypertension but does prevent cardiovascular disease
72
Q

For which population are alpha antagonists first line for blood pressure management?

A

those with comorbid BPH

73
Q

What hypertensive medications are safe in pregnancy?

A
  • beta blockers are first choice
  • calcium channel blockers
  • hydralazine
  • methyldopa
74
Q

For which populations are beta blockers first line for hypertension?

A
  • pregnant women
  • those with comorbid hyperthyroidism
  • those with coronary artery disease
75
Q

How is hypertensive crisis defined and treated?

A
  • defined as hypertension with end-organ damage in the form of confusion, vision change, dyspnea, or chest pain
  • treat with labetalol or nitroprusside

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