Endocrine Disorders, Hypertension, Hypercholesterolemia, Acquired Heart Disease, and Cardiovascular Disease Flashcards
prevalence of DM in USA
8%
leading cause of new cases of blindness in American adults 20-74 years
DM
which hormone(s) decrease and increase blood glucose, respectively?
decrease: insulin
increase: glucagon, cortisol, adrenocorticotropin, epinephrine, thyroxine, somatotropin
what accounts for the decreased insulin sensitivity in type II diabetes?
decrease in the number of insulin receptors
Diagnostic criteria for T2DM
Any 1 of the following criteria met on two separate days:
- HbA1c greater than or equal to 6.5%
- FPG greater than or equal to 126 mg/dL
- 2-hour plasma glucose level greater than or equal to 200 mg/dL after 75 g OGT test
- random plasma glucose greater than or equal to 200 mg/dL in a patient with classic symptoms (polyphagia, polydipsia, polyuria)
% of patients w/ T1DM that present after 35 years of age?
25%
mechanism of T1DM
destruction of insulin-producing pancreatic beta cells, usually autoimmune
screening recommendations for patients with no risk factors or suggestive signs or symptoms of diabetes?
start at 45, then every 3 years if still normal
percentage of DM in USA that is type II?
90%
percentage of T2DM patients wit obesity?
80-90
non obesity risk factors for T2DM?
hypertension, gestational diabetes, physical inactivity, low socioeconomic status
prevalence of gestational diabetes in USA? percentage of patients with gestational DM who develop T2DM by 10 years?
4% of all pregnancies in USA
30-50%
criteria for impaired glucose tolerance, impaired fasting glucose, and pre-diabetes by HbA1c?
FG: >/=110
IGT: >/=140
A1c >/= 5.7 (or 6.0, depending on source…)
HbA1c goal for diabetic patients?
7.0
name the different types of insulin therapy with the specific drugs in each class. also state onset of action for each type
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
what are the Somogyi phenomenon and the dawn phenomenon?
Somogyi: rebound hyperglycemia after episode of hypoglycemia (can make insulin self-dosing difficult)
dawn: early morning hyperglycemia, likely from growth hormone secreted during sleep
treatment of acute hypoglycemia?
sugary food/drink if able to swallow. otherwise, 25g iv glucose or 1mg subQ glucagon
after diet and exercise, what is the first line treatment for T2DM? MOA?
Metformin (biguanide). Unknown, but ultimately increases insulin sensitivity
what oral medication class has the greatest efficacy in glycemic lowering, and what is its MOA?
sulfonylureas. increase pancreatic insulin secretion
contraindications to sulfonylureas
pregnancy, and any history of prior ketoacidosis
most significant adverse effect of sulfonylureas?
hypoglycemia
common side effect of Metformin? more severe side effect?
GI upset. lactic acidosis
contraindications to Metformin? special precautions when taking Metformin?
Renal insufficiency.
Given risk of lactic acidosis, hold Metformin prior to receiving iodinated contrast and hold prior to surgery
mechanism and common side effect of alpha-glucosidase inhibitors?
delay absorption of carbohyrates. flatulence
mechanism and side effects of thiazolidinediones
increase insulin sensitivity and decrease hepatic gluconeogenesis. can cause fluid retention resulting in cardiovascular complications. also have increased rates of diabetic macular edema
mechanisms of GLP-1 agonists, DPP-IV inhibitors, and SGLT2 inhibitors
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
main difference between nonketotic hyperglycemic hyperosmolar coma and DKA?
ketoacids are formed in DKA (glucose can not enter cells due to very little or no insulin, leading to a superimposed metabolic acidosis)
diagnostic cutoff for diabetic nephropathy?
albuminuria >/= 300 mg/24 h
describe the pathway for thyroid hormone action
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.
screening recommendations for thyroid disease?
TSH and free T4
laboratory risk factors for TED in Graves?
high thyroid stimulating immunoglobulin and absence of thyroperoxidase antibody
T or F:
- Graves has a 10:1 female preponderance
- thyroid stimulating immunoglobulin levels correlate with the severity of clinical disease in Graves
- Peaks in 5th and 6th decade of life
- stress and cigarette smoking are risk factors
- T
- T
- F (3rd and 4th decade)
- T
proportion of Graves patients who have clinically obvious TED at time of diagnosis?
1/3
treatments for Graves. which treatment can worsen TED, and what can you co-administer to help ameliorate this?
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
most common type of thyroid cancer? worst prognosis? associated with MEN 2?
papillary. anaplastic. medullary
hormones of hypothalamus and their effects
TRH: inc TSH and prolactin GnRH: inc FSH and LH GHRH: inc GH somatostatin: dec GH and TSH CRH: inc ACTH dopamin: dec prolactin
sudden onset excruciating headache, visual field loss, diplopia, and marked hypotension on arrival to ED
pituitary apoplexy
features of MEN 1
parathyroid adenoma, pancreatic adenoma, pituitary adenoma
features of MEN 2a and 2b
2a: medullary thyroid cancer, pheochromocytoma, hyperparathyroidism
2b: med thyroid ca, pheo, ganglioneuromas (can affect eyelids and conj), marfanoid body habitus, prominent corneal nerves
normal BP
BP treatment goal for 18-59 years old
BP treatment goal for 60 and older
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
describe the risk of cardiovascular disease as results to incremental increases in BP above normal
risk doubles with each 20/10 increase starting at 115/75
when is combination therapy indicated in treatment of hypertension?
when 20/10 or more above goal with monotherapy
prehypertension
stage 1 HTN
stage 2 HTN
120-139/80-89
140-159/90-99
160/100 and above
briefly outline the RAAS
renin –(angiotensinogen)–> angiotensin 1 –(ACE)–> angiotensin II –> aldosterone production, vasoconstriction, sodium retention
name a common OTC drug that can lead to HTN
NSAIDs (via fluid retention)
name 5 lifestyle modifications that have been shown to improve BP control
weight loss, DASH diet, decreased ethanol consumption, dietary sodium reduction, physical activity
general summary of first line treatment options for HTN according to JNC 8
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)
MOA of thiazide, loop diuretic, ACEi, ARB, CCB, beta-blocker
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
side effects and indications for diuretics
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
side effects and indications for ACE inhibitors
Dry cough most common. Also angioedema. C/I in pregnancy. Beneficial for patients with LV dysfunction, diabetes, and kidney disease
In which patients should you avoid beta blockers
asthmatics, 2nd-3rd degree heart block,
antihypertensive medication commonly used in pregnancy?
methyldopa
T or F: low dose therapy with 2 antihypertensives are associated with less side effects than high dose monotherapy
True
oral drug of choice for hypertensive emergency?
sodium nitroprusside or nitroglycerine
Antihypertensive(s) of choice for the following:
- stable angina pectoris
- HF w/ systolic dysfunction
- diabetic nephropathy
- h/o stroke
- elderly patient with isolated systolic HTN
- pregnancy
- blacks
- beta bockers
- beta blockers and ACE inhibitors
- ACE inhibitors and ARBs
- combination of ACE inhibitor and thiazide
- diuretic +/- beta blocker, or CCB alone
- methyldopa, beta blockers, and vasodilators (ACE inhibitors and ARBs contraindicated)
- diuretics and CCBs
what are preeclampsia and eclampsia
preeclampsia: pregnancy, HTN, proteinuria, generalized edema +/ - coag abnormalities
eclampsia = above + generalized seizures
Discuss the four grades of hypertensive retinopathy
- None
- Mild: AV nicking, arterial narrowing, copper wiring
- Moderate: hemorrhage, MA, cotton wool spot, hard exudate
- Malignant: moderate + disc swelling
First, second, and third leading causes of death in the US
- heart disease
- cancer
- stroke
most recent cholesterol and lipid guidlines
total cholesterol < 200, TG < 150, LDL < 100, HDL > 60
side effects of statins
myopathy, elevated transaminases, diarrhea, liver failure, polyneuropathy
number one preventable risk factor for cardiovascular disease worldwide?
smoking
ST depression and/or T wave inversion with negative troponins? With troponins? ST elevation and troponins?
unstable angina. NSTEMI (partial thickness myocardial necrosis). STEMI (full thickness necrosis)
management of acute MI
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)
Overall most sensitive and specific cardiac biomarkers for MI? In first 6-9 hours? For delayed presentation of MI?
troponins T and I. CK-MB. troponins T and I (remain elevated from 3 hours to 14 days)
medical management of NSTEMI
beta blocker, ACE inhibitor, nitrates, dual antiplatelet therapy, antithrombin therapy
normal ejection fraction? In mild, moderate, and severe CHF?
normal >50%
mild 40-49%
moderate 25-39%
severe
what determines afterload for the right and left ventricles
right: pulmonary artery pressure
left: aortic pressure
systolic v diastolic dysfunction
systolic: anything that affects preload, afterload, or contractility
diastolic: impaired ventricular relaxation
first line medical treatment for CHF
ACE inhibitor and diuretic
systolic dysfunction is improved by decreasing ____ and diastolic dysfunction is improved by decreasing____
afterload
preload
treatment of choice for recurrent V-tach
Amiodarone
treatment for sustained V-tach with hemodynamic compromise
immediate synchnozed DC cardioversion
treatment for V-fib
immediate unsynchronized DC cardioversion
ocular side effects of amiodarone
corneal verticillata, photosensitivity, periocular skin discoloration, and rarely optic neuropathy
ocular side effects of systemic beta blockers
lower IOP, keratoconjunctivitis sicca-like syndrome, visual disturbances or hallucinations
ocular side effects of digoxin
glare, disturbances of color vision, flashing lights
what is the leading cause of long-term disability in the USA?
stroke
time cut-off to receive TPA after a stroke?
4 1/2 hours
% 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?
70-99%
50-99%, depending on patient-specific factors
3%
workup of acute stroke
CBC, BMP, coags, CT non-con
what antiplatelet has been shown to improve mortality if given within 48 hours of a stroke
Aspirin
T or F: heparin is useful in the treatment of an acute non—hemorrhagic stroke
false
T or F: the presence of a carotid bruit is a better predictor of arteriosclerotic disease than that of a stroke
true
most common site for a berry aneurysm, and what signs/symptoms will a patient have if this ruptures?
origin of PCom from ICA. headache and pupil-involving 3rd nerve palsy
All of the following intracranial vascular malformations have low bleeding risk EXCEPT: capillary telangiectasia cavernous angioma venous angioma AVM
AVM
what is the definitive test to diagnose an intracranial AVM?
cerebral arteriography
What should you do if you have high suspicion for SAH but CT is negative?
lumbar puncture
