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MY UPDATE ON GEN MEDICINE > Endocrine Disorders, Hypertension, Hypercholesterolemia, Acquired Heart Disease, and Cardiovascular Disease > Flashcards

Endocrine Disorders, Hypertension, Hypercholesterolemia, Acquired Heart Disease, and Cardiovascular Disease Flashcards

1
Q

prevalence of DM in USA

A

8%

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2
Q

leading cause of new cases of blindness in American adults 20-74 years

A

DM

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3
Q

which hormone(s) decrease and increase blood glucose, respectively?

A

decrease: insulin
increase: glucagon, cortisol, adrenocorticotropin, epinephrine, thyroxine, somatotropin

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4
Q

what accounts for the decreased insulin sensitivity in type II diabetes?

A

decrease in the number of insulin receptors

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5
Q

Diagnostic criteria for T2DM

A

Any 1 of the following criteria met on two separate days:

  1. HbA1c greater than or equal to 6.5%
  2. FPG greater than or equal to 126 mg/dL
  3. 2-hour plasma glucose level greater than or equal to 200 mg/dL after 75 g OGT test
  4. random plasma glucose greater than or equal to 200 mg/dL in a patient with classic symptoms (polyphagia, polydipsia, polyuria)
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6
Q

% of patients w/ T1DM that present after 35 years of age?

A

25%

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7
Q

mechanism of T1DM

A

destruction of insulin-producing pancreatic beta cells, usually autoimmune

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8
Q

screening recommendations for patients with no risk factors or suggestive signs or symptoms of diabetes?

A

start at 45, then every 3 years if still normal

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9
Q

percentage of DM in USA that is type II?

A

90%

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10
Q

percentage of T2DM patients wit obesity?

A

80-90

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11
Q

non obesity risk factors for T2DM?

A

hypertension, gestational diabetes, physical inactivity, low socioeconomic status

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12
Q

prevalence of gestational diabetes in USA? percentage of patients with gestational DM who develop T2DM by 10 years?

A

4% of all pregnancies in USA

30-50%

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13
Q

criteria for impaired glucose tolerance, impaired fasting glucose, and pre-diabetes by HbA1c?

A

FG: >/=110
IGT: >/=140
A1c >/= 5.7 (or 6.0, depending on source…)

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14
Q

HbA1c goal for diabetic patients?

A

7.0

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15
Q

name the different types of insulin therapy with the specific drugs in each class. also state onset of action for each type

A 
rapid-acting (15 min): aspart, glulisine, lispro
regular/short acting (30 min): regular human insulin
intermediate acting (2-4 hr): insulin isophane suspension
long-acting (several hrs): glargine, detemir
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16
Q

what are the Somogyi phenomenon and the dawn phenomenon?

A

Somogyi: rebound hyperglycemia after episode of hypoglycemia (can make insulin self-dosing difficult)

dawn: early morning hyperglycemia, likely from growth hormone secreted during sleep

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17
Q

treatment of acute hypoglycemia?

A

sugary food/drink if able to swallow. otherwise, 25g iv glucose or 1mg subQ glucagon

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18
Q

after diet and exercise, what is the first line treatment for T2DM? MOA?

A

Metformin (biguanide). Unknown, but ultimately increases insulin sensitivity

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19
Q

what oral medication class has the greatest efficacy in glycemic lowering, and what is its MOA?

A

sulfonylureas. increase pancreatic insulin secretion

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20
Q

contraindications to sulfonylureas

A

pregnancy, and any history of prior ketoacidosis

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21
Q

most significant adverse effect of sulfonylureas?

A

hypoglycemia

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22
Q

common side effect of Metformin? more severe side effect?

A

GI upset. lactic acidosis

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23
Q

contraindications to Metformin? special precautions when taking Metformin?

A

Renal insufficiency.

Given risk of lactic acidosis, hold Metformin prior to receiving iodinated contrast and hold prior to surgery

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24
Q

mechanism and common side effect of alpha-glucosidase inhibitors?

A

delay absorption of carbohyrates. flatulence

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25
Q

mechanism and side effects of thiazolidinediones

A

increase insulin sensitivity and decrease hepatic gluconeogenesis. can cause fluid retention resulting in cardiovascular complications. also have increased rates of diabetic macular edema

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26
Q

mechanisms of GLP-1 agonists, DPP-IV inhibitors, and SGLT2 inhibitors

A

GLP-1 agonists act like incretins and therefore increase post-prandial insulin, decrease post-prandial glucagon and increase satiety. DPP-IV inhibitors decrease the breakdown of natural incretins.
SGLT2 inhibitors lower the threshold of urinary glucose excretion

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27
Q

main difference between nonketotic hyperglycemic hyperosmolar coma and DKA?

A

ketoacids are formed in DKA (glucose can not enter cells due to very little or no insulin, leading to a superimposed metabolic acidosis)

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28
Q

diagnostic cutoff for diabetic nephropathy?

A

albuminuria >/= 300 mg/24 h

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29
Q

describe the pathway for thyroid hormone action

A

TRH (hypothalamus) –> TSH (anterior pituitary) –> release of T4 and T3 from thyroid. T4 is de-iodinated in liver and kidneys. T3 is active form. 99.7% of T3 is rendered inactive by binding to TBG in blood. Remainder of active T3 regulates tissue metabolism including CNS development and bone growth. T3 and T4 negatively feed back on TSH.

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30
Q

screening recommendations for thyroid disease?

A

TSH and free T4

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31
Q

laboratory risk factors for TED in Graves?

A

high thyroid stimulating immunoglobulin and absence of thyroperoxidase antibody

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32
Q

T or F:

  1. Graves has a 10:1 female preponderance
  2. thyroid stimulating immunoglobulin levels correlate with the severity of clinical disease in Graves
  3. Peaks in 5th and 6th decade of life
  4. stress and cigarette smoking are risk factors
A
  1. T
  2. T
  3. F (3rd and 4th decade)
  4. T
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33
Q

proportion of Graves patients who have clinically obvious TED at time of diagnosis?

A

1/3

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34
Q

treatments for Graves. which treatment can worsen TED, and what can you co-administer to help ameliorate this?

A

B-blocker for symptoms, PTU or methimazole, radioactive iodine (I 131), partial thyroidectomy

Radioactive Iodine can worsen TED, but corticosteroids can help prevent this side effect

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35
Q

most common type of thyroid cancer? worst prognosis? associated with MEN 2?

A

papillary. anaplastic. medullary

36
Q

hormones of hypothalamus and their effects

A 
TRH: inc TSH and prolactin
GnRH: inc FSH and LH
GHRH: inc GH
somatostatin: dec GH and TSH
CRH: inc ACTH
dopamin: dec prolactin
37
Q

sudden onset excruciating headache, visual field loss, diplopia, and marked hypotension on arrival to ED

A

pituitary apoplexy

38
Q

features of MEN 1

A

parathyroid adenoma, pancreatic adenoma, pituitary adenoma

39
Q

features of MEN 2a and 2b

A

2a: medullary thyroid cancer, pheochromocytoma, hyperparathyroidism
2b: med thyroid ca, pheo, ganglioneuromas (can affect eyelids and conj), marfanoid body habitus, prominent corneal nerves

40
Q

normal BP
BP treatment goal for 18-59 years old
BP treatment goal for 60 and older

A

less than 120/80
**less than 130/80 if also have diabetes or renal disease
less than 140 systolic and 90 diastolic
less than 150 systolic and 90 diastolic

41
Q

describe the risk of cardiovascular disease as results to incremental increases in BP above normal

A

risk doubles with each 20/10 increase starting at 115/75

42
Q

when is combination therapy indicated in treatment of hypertension?

A

when 20/10 or more above goal with monotherapy

43
Q

prehypertension
stage 1 HTN
stage 2 HTN

A

120-139/80-89
140-159/90-99
160/100 and above

44
Q

briefly outline the RAAS

A

renin –(angiotensinogen)–> angiotensin 1 –(ACE)–> angiotensin II –> aldosterone production, vasoconstriction, sodium retention

45
Q

name a common OTC drug that can lead to HTN

A

NSAIDs (via fluid retention)

46
Q

name 5 lifestyle modifications that have been shown to improve BP control

A

weight loss, DASH diet, decreased ethanol consumption, dietary sodium reduction, physical activity

47
Q

general summary of first line treatment options for HTN according to JNC 8

A

non-black patients: any of the following classes: thiazides, CCBs, ACE inhibitors, ARBs

black patients: either thiazide or CCB

*beta blockers are not first line (less stroke prevention)

48
Q

MOA of thiazide, loop diuretic, ACEi, ARB, CCB, beta-blocker

A

thiazide: increase sodium load on kidney’s distal tubule leading to natriuresis and ultimately decreased peripheral vascular resistance
loop: block sodium resorption at ascending loop of Henle

ACEi: block conversion of angiotensin I to II, preventing its potent vasoconstriction

ARB: block angiotensin receptors thereby preventing its vasoconstriction and aldosterone secreting effects

CCB: block Ca entry into vascular smooth muscle, thereby decreasing myocardial contractility and systemic vascular resistence

beta-blockers: block beta 1 and or beta 2 receptors leading to inhibition of decreased heart rate, decreased myocardial contractility, peripheral vasodilation, and bronchoconstriction

49
Q

side effects and indications for diuretics

A

Loops and thiazides cause electrolyte abnormalities. Thiazides cause hyperglycemia and hyperlipidemia, although duel therapy with ACE inhibitors can reduce these side effects. Diuretics are particularly useful for patients with salt-sensitive hypertension like blacks and the elderly

50
Q

side effects and indications for ACE inhibitors

A

Dry cough most common. Also angioedema. C/I in pregnancy. Beneficial for patients with LV dysfunction, diabetes, and kidney disease

51
Q

In which patients should you avoid beta blockers

A

asthmatics, 2nd-3rd degree heart block,

52
Q

antihypertensive medication commonly used in pregnancy?

A

methyldopa

53
Q

T or F: low dose therapy with 2 antihypertensives are associated with less side effects than high dose monotherapy

A

True

54
Q

oral drug of choice for hypertensive emergency?

A

sodium nitroprusside or nitroglycerine

55
Q

Antihypertensive(s) of choice for the following:

  1. stable angina pectoris
  2. HF w/ systolic dysfunction
  3. diabetic nephropathy
  4. h/o stroke
  5. elderly patient with isolated systolic HTN
  6. pregnancy
  7. blacks
A
  1. beta bockers
  2. beta blockers and ACE inhibitors
  3. ACE inhibitors and ARBs
  4. combination of ACE inhibitor and thiazide
  5. diuretic +/- beta blocker, or CCB alone
  6. methyldopa, beta blockers, and vasodilators (ACE inhibitors and ARBs contraindicated)
  7. diuretics and CCBs
56
Q

what are preeclampsia and eclampsia

A

preeclampsia: pregnancy, HTN, proteinuria, generalized edema +/ - coag abnormalities

eclampsia = above + generalized seizures

57
Q

Discuss the four grades of hypertensive retinopathy

A
  1. None
  2. Mild: AV nicking, arterial narrowing, copper wiring
  3. Moderate: hemorrhage, MA, cotton wool spot, hard exudate
  4. Malignant: moderate + disc swelling
58
Q

First, second, and third leading causes of death in the US

A
  1. heart disease
  2. cancer
  3. stroke
59
Q

most recent cholesterol and lipid guidlines

A

total cholesterol < 200, TG < 150, LDL < 100, HDL > 60

60
Q

side effects of statins

A

myopathy, elevated transaminases, diarrhea, liver failure, polyneuropathy

61
Q

number one preventable risk factor for cardiovascular disease worldwide?

A

smoking

62
Q

ST depression and/or T wave inversion with negative troponins? With troponins? ST elevation and troponins?

A

unstable angina. NSTEMI (partial thickness myocardial necrosis). STEMI (full thickness necrosis)

63
Q

management of acute MI

A

morphine, O2, nitrates, aspirin, plavix, heparin, beta blocker, and immediate coronary angiography and primary PCI (w/in 90 minutes). If PCI cannot be done within 90 minutes, then immediate thrombolysis is recommended. No NSAIDs! (they increase mortality)

64
Q

Overall most sensitive and specific cardiac biomarkers for MI? In first 6-9 hours? For delayed presentation of MI?

A

troponins T and I. CK-MB. troponins T and I (remain elevated from 3 hours to 14 days)

65
Q

medical management of NSTEMI

A

beta blocker, ACE inhibitor, nitrates, dual antiplatelet therapy, antithrombin therapy

66
Q

normal ejection fraction? In mild, moderate, and severe CHF?

A

normal >50%
mild 40-49%
moderate 25-39%
severe

67
Q

what determines afterload for the right and left ventricles

A

right: pulmonary artery pressure
left: aortic pressure

68
Q

systolic v diastolic dysfunction

A

systolic: anything that affects preload, afterload, or contractility
diastolic: impaired ventricular relaxation

69
Q

first line medical treatment for CHF

A

ACE inhibitor and diuretic

70
Q

systolic dysfunction is improved by decreasing ____ and diastolic dysfunction is improved by decreasing____

A

afterload

preload

71
Q

treatment of choice for recurrent V-tach

A

Amiodarone

72
Q

treatment for sustained V-tach with hemodynamic compromise

A

immediate synchnozed DC cardioversion

73
Q

treatment for V-fib

A

immediate unsynchronized DC cardioversion

74
Q

ocular side effects of amiodarone

A

corneal verticillata, photosensitivity, periocular skin discoloration, and rarely optic neuropathy

75
Q

ocular side effects of systemic beta blockers

A

lower IOP, keratoconjunctivitis sicca-like syndrome, visual disturbances or hallucinations

76
Q

ocular side effects of digoxin

A

glare, disturbances of color vision, flashing lights

77
Q

what is the leading cause of long-term disability in the USA?

A

stroke

78
Q

time cut-off to receive TPA after a stroke?

A

4 1/2 hours

79
Q

% stenosis where CEA is recommended in asymptomatic patients? Symptomatic patient (recent TIA or stroke)?What is the minimum morbidty at a stroke center recommended to perform CEA in these settings?

A

70-99%
50-99%, depending on patient-specific factors
3%

80
Q

workup of acute stroke

A

CBC, BMP, coags, CT non-con

81
Q

what antiplatelet has been shown to improve mortality if given within 48 hours of a stroke

A

Aspirin

82
Q

T or F: heparin is useful in the treatment of an acute non—hemorrhagic stroke

A

false

83
Q

T or F: the presence of a carotid bruit is a better predictor of arteriosclerotic disease than that of a stroke

A

true

84
Q

most common site for a berry aneurysm, and what signs/symptoms will a patient have if this ruptures?

A

origin of PCom from ICA. headache and pupil-involving 3rd nerve palsy

85
Q 
All of the following intracranial vascular malformations have low bleeding risk EXCEPT:
capillary telangiectasia
cavernous angioma
venous angioma
AVM
A

AVM

86
Q

what is the definitive test to diagnose an intracranial AVM?

A

cerebral arteriography

87
Q

What should you do if you have high suspicion for SAH but CT is negative?

A

lumbar puncture

MY UPDATE ON GEN MEDICINE (3 decks)

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