General Medicine Flashcards
Sample size of a study must be large enough to reject __, which is that no difference exists in the group that received the intervention compared with the group that did not.
Null hypothesis
Power of a study depends on these three factors
Sample size, expected difference in outcome of interest between groups, variability of outcome of interest (standard deviation)
This occurs when a researcher expects a different result in intervention group and adjusts his measurement of the outcome of interest to satisfy this expectation.
Investigator bias
This is the appropriate statistical test to compare an intervention and control group if data are normally distributed and continuous (ex: macular thickness)
Student’s t-test
This is an appropriate statistical test to compare an intervention and control group if data are not normally distributed but are continuous
Wilcoxon rank sum test
This statistical test can be used for categorical data (present or absent; small, medium, or large)
Chi-square test
This is the percentage of those who have disease and also have abnormal test results
Sensitivity
This is the percentage of disease-free people with normal test results
Specificity
This is the percentage of those with disease + abnormal test and all those with an abnormal test
Positive predictive value
This is the percentage of disease-free people + negative test and all those with a negative test
Negative predictive value
This is a graphical representation of sensitivity and specificity, where sensitivity is on the y-axis and (1 - specificity) is on the x-axis.
Receiver operating characteristic (ROC) curve
These six hormones increase plasma glucose levels.
Somatotropin, adrenocorticotropin, cortisol, epinephrine, glucagon, thyroxine
Diagnosis of diabetes is made with one of these four criteria (confirmed with retesting on a subsequent day)
HbA1c >/= 6.5%, FPG >/=126 mg/dL, 2hr gluc >/=200 (75g OGTT), random gluc >/= 200 w/ symptoms
Fasting plasma glucose level and 2-hour, 75g OGTT results diagnostic of impaired glucose tolerance (IGT)
Fasting gluc 110-126, 2-hr 75g OGTT 140-200
This is the occurrence of rebound hyperglycemia after hypoglycemia.
Somogyi phenomenon
This occurs when a normal physiologic process is exaggerated, resulting in substantial hyperglycemia (characterized by early-morning hyperglycemia not preceded by hypoglycemia or waning of insulin -> surge of GH shortly after falling asleep)
Dawn phenomenon
Symptoms of this include: palpitations, perspiration, pallor, tachycardia, HTN, dilated pupils (from hyperepinephrinemia); HA, paresthesia, blurred vision, drowsiness, irritability, bizarre behavior, AMS, combativeness (neurologic manifestations).
Hypoglycemia
These are three second-generation sulfonylureas, which reduce HbA1c by 0.5-1.5%. They are inexpensive and act by stimulating pancreatic insulin secretion. ADE: hypoglycemia, weight gain.
Glimepiride, glipizide, glyburide
This is a biguanide medication that is used first-line in the treatment of DM2; it reduces HbA1c by 1.5%. It increases insulin sensitivity and can lead to modest weight loss. ADE: GI upset, metallic taste, lactic acidosis.
Metformin
These are two alpha-glucosidase inhibitors, which reduce HbA1c by 0.5-0.8%. They delay absorption of carbs by inhibiting the breakdown of complex carbs into monosaccharides. ADE: flatulence.
Acarbose, miglitol
These are two thiazolidinediones, which reduce HbA1c by 0.5-1.4%. They increase insulin sensitivity in muscle and adipose tissue and inhibit hepatic gluconeogenesis. ADE: weight gain, fluid retention with CV complications, higher rates of DME.
Pioglitazone, rosiglitazone
These are two meglitinides, which reduce HbA1c by 0.5-1.5%. Their mechanisms and ADEs are similar to sulfonylureas.
Nateglinide, repaglinide
These are three glucagon-like peptide-1 (GLP-1) agonists, which reduce HbA1c by 0.5-1.0%. They are incretin mimetics that enhance pancreatic insulin secretion, inhibit glucagon secretion, and promote satiety. ADE: GI upset, pancreatitis, thyroid C-cell tumor development.
Exenatide, liraglutide, lixisenatide
These are four dipeptidyl-peptidase IV (DPP-IV) inhibitors, which reduce HbA1c by 0.7-1.2%. DPP-IV normally deactivates incretins, so these medications function similarly to GLP-1 agonists. They are expensive.
Linagliptin, saxagliptin, sitagliptin, vildagliptin
These are two sodium-glucose transporter-2 (SGLT2) inhibitors, which reduce HbA1c by 0.6-1.0%. They increase urinary glucose excretion, leading to weight loss and improved glucose levels. ADE: hypotension, dehydration, UTI.
Canagliflozin, dapagliflozin
These cells secrete calcitonin and play a role in calcium homeostasis.
Parafollicular (or C) cells
These are made up of a single layer of epithelial cells surrounding colloid, which consists mostly of thyroglobulin, the storage form of T4 and T3.
Thyroid follicles
This is the main secretory product of the thyroid gland.
T4 (thyroxine)
This is the metabolically active form of thyroid hormone, 80% of which is created by deiodination of its predecessor in the liver and kidneys and 20% of which is secreted directly by the thyroid gland.
T3 (triiodothyronine)
These two thyroid tests are elevated in pregnancy and with OCP use.
TBG and total T4 (free T4 remains WNL)
This antibody is found in 95% of patients with Hashimoto thyroiditis, 55% of patients with Graves, and 10% of adults with no apparent thyroid disease.
Thyroid microsomal antibody
High serum levels of thyroid-stimulating Ig and the absence of thyroperoxidase antibody are both risk factors for this complication of Graves disease.
Thyroid (Graves)-associated ophthalmopathy
Clinical findings of _ include exophthalmos, chest palpitations, excessive sweating, diarrhea, weight loss, heat sensitivity. It can progress to _, which is often precipitated by surgery, infection, or trauma and presents with fever, tachycardia, n/v, agitation, and psychosis. Patients can become comatose 2/2 hypotension, and it is fatal if untreated.
Hyperthyroidism (thryotoxicosis); thyroid storm
This is brawny, non-pitting swelling of the pretibial area, ankles, or feet that is almost always associated with thyroid eye disease.
Infiltrative dermopathy
This is non-pitting edema caused by subcutaneous accumulation of mucopolysaccharides in severe cases of hypothyroidism.
Myxedema
This is manifested by weakness, fatigue, memory loss, dry skin, hair loss, deepening of the voice, weight gain (despite loss of appetite), cold intolerance, arthralgias, constipation, and muscle cramps.
Hypothyroidism
This is the most common form of thyroid cancer. There appears to have no adverse effect on survival if removed before extension outside the capsule of the gland.
Papillary carcinoma
Like papillary carcinoma, this thyroid cancer is associated with a normal lifespan if identified before it becomes invasive, but late metastases can occur.
Follicular carcinoma
This thyroid cancer arises from C cells and produces calcitonin. It can occur as a solitary malignant tumor or as part of MEN 2.
Medullary carcinoma
This rare tumor is the most malignant tumor of the thyroid gland, found mainly in patients >60 y/o. In the giant cell form, survival is <6 months from the time of diagnosis. In the small cell form, 5-year survival is 20-25%.
Anaplastic carcinoma
Size of pituitary microadenomas vs macroadenomas
micro: <10mm; macro: >/= 10mm
This results from hemorrhage or infarction in a pituitary adenoma. Symptoms include sudden excruciating HA, visual field loss, diplopia (pressure on oculomotor nerves), and hypopituitarism (including hypocortisolism). Reduced vision and AMS are indications for transsphenoidal surgical decompression.
Pituitary apoplexy
This is characterized by parathyroid, enteropancreatic, and pituitary tumors. S/S include hyperparathyroidism, Zollinger-Ellison syndrome, insulinomas, prolactinomas, etc. Carcinoid and adrenal tumors can develop as well.
Multiple endocrine neoplasia type 1 (MEN 1)
This is characterized by medullary thyroid carcinoma, pheochromocytoma, and hyperparathyroidism.
Multiple endocrine neoplasia type 2a (MEN 2a)
This is characterized by medullary thyroid carcinoma, ganglionomas (on lips, eyelids, and tongue), pheochromocytoma, and marfanoid features (pectus excavatum and scoliosis but without lens subluxation or aortic disease). Patients also have prominent corneal nerves in a clear stroma (100% of patients), making ophthalmologists potentially instrumental in early diagnosis.
Multiple endocrine neoplasia type 2b (MEN 2b)
This secondary cause of HTN presents with a flank mass.
Polycystic kidney disease
This secondary cause of HTN presents with unilateral abd bruit in a young patient with marked HTN; new-onset HTN with severe end-organ disease
Renovascular disease
This secondary cause of HTN presents with markedly labile BP with tachycardia and HA.
Pheochromocytoma
This secondary cause of HTN presents with persistent hypokalemia in the absence of diuretic therapy or marked drop with low-dose diuretics.
Hyperaldosteronism
This secondary cause of HTN presents with delayed or absent femoral pulses in a young patient.
Coarctation of the aorta
This secondary cause of HTN presents with truncal obesity and abdominal striae
Cushing syndrome
BP goal in DM or renal disease
<130/80
These medications increase sodium load in the distal tubules and initially decrease plasma volume and cardiac output through natriuresis. As the RAAS compensates for decreased plasma volume, CO returns to normal and PVR is lowered.
Thiazide-type diuretics (chlorothiazide, chlorthalidone, HCTZ)
These medications act on the ascending loop of Henle and block sodium resorption, causing an initial decrease in plasma volume. BP is eventually lowered due to decreased PVR. They are used in pts with moderate renal insufficiency.
Loop diuretics (furosemide, bumatenide, torsemide)
These medications competitively block the action of aldosterone to prevent potassium loss from the distal tubule, or they act directly on the distal tubule to inhibit aldosterone-induced sodium resorption in exchange for potassium.
Potassium-sparing diuretics (amiloride, triamterene, eplerenone, spironolactone)
The ADE of these medications include a dry cough, angioneurotic edema, hypotension, hyperkalemia, abnormal taste, leukopenia, proteinuria, and renal failure (in pts with pre-existing renal insufficiency). They should be avoided in pts with angioedema, and they are contraindicated in pregnancy (adverse effects on fetal renal function, fetal death)
Angiotensin-converting enzyme (ACE) inhibitors (benazepril, captopril, enalapril, fosinopril, lisinopril)
These medications cause fewer ADEs than ACE inhibitors (no cough), and angioedema is rare. They are also contraindicated in pregnancy.
Angiotensin II receptor blockers (ARBs) (candesartan, irbesartan, losartan)
These medications act by blocking entry of calcium into vascular smooth muscles, leading to decreased myocardial contractility and decreased SVR. ADE include constipation, HA, fatigue, dizziness, nausea, palpitations, flushing, edema, gingival hyperplasia, arrhytmias, and cardiac ischemia.
Calcium channel blockers (non-dihydropyridines: diltiazem, verapamil; dihydropyridines: amlodipine, nicardipine, nifedipine)
These two medications have both alpha- and beta-blocking properties, so in addition to acting as a beta blocker, they produce additional vasodilatory effects.
Carvedilol, labetalol
These medications have a “first-dose effect,” in which BP is decreased more with the initial dose than with subsequent doses. They can also cause orthostatic hypotension, HA, dizziness, and drowsiness.
Alpha-1 blockers (dexazosin, prazosin, terazosin)
These are potent, central-acting anti-hypertensive that decrease sympathetic tone, cardiac output, and PVR. ADE: fluid retention, dry mouth, dizziness, orthostatic hypotension, rash, impotence, hepatitis, positive Coombs and ANA test, and heart failure in patients with left ventricular dysfunction.
Alpha-2 agonists (and other centrally acting drugs) (clonidine, guanfacine, methyldopa, reserpine)
These are two direct-acting vasodilators that decrease PVR. They are generally reserved for pregnancy or intractable HTN. They should be used with caution in ischemic heart disease. ADE: HA, tachycardia, edema, n/v, lupus-like syndrome, hypertrichosis.
Minoxidil, hydralazine
This is a direct renin inhibitor used to treat HTN. It is more likely to be effective in young, white patients or in any patients receiving diuretics or CCBs (renin system activation). ADE: diarrhea.
Aliskiren
This is defined as the presence of central obesity and two of the following: triglyceride >150, reduced HDL, SBP >130 or DBP >85, fasting gluc >100.
Metabolic syndrome
This is characterized by pregnancy, HTN, proteinuria, generalized edema, and possibly coagulation and liver function abnormalities after 20wks gestation
Preeclampsia (eclampsia = preeclampsia + generalized seizures)
This grade of hypertensive retinopathy is characterized by arteriolar narrowing, AV nicking, opacity (“copper wiring” due to thickening of arteriolar wall, or a combination of these.
Mild
This grade of hypertensive retinopathy is characterized by hemorrhage (blot, dot, or flame-shaped), microaneurysm, cotton-wool spot, hard exudates, or a combination of these signs.
Moderate
This grade of hypertensive retinopathy is characterized by signs of moderate retinopathy (hemorrhage, microaneurysms, cotton-wool spots, and/or hard exudates) plus swelling of the optic disc.
Malignant
This is manifested by precordial chest pain or tightness often triggered by physical exertion, emotional distress, or eating. It is due to atherosclerotic heart disease. It typically lasts 5-10 minutes, it is relieved by rest and/or nitroglycerin, and its pattern of symptoms have not changed substantially over >3 months.
Stable angina pectoris
This is manifested by precordial chest pain or tightness that occurs at rest and is not related to physical exertion. There are ST elevations on ECG during pain episodes, which are caused by coronary artery vasospasms. Underlying atherosclerosis is present in 60-80% of cases, and thrombosis/occlusion may result during one of these episodes.
Variant (Prinzmetal) angina
These are four direct thrombin inhibitors that can be used in acute coronary syndrome or for other conditions requiring anticoagulation.
Hirudin, bivalirudin, argatroban, dabigatran
These are three glycoprotein IIb/IIIa inhibitors that have been shown to reduce the risk of death and MI in patients with NSTEMI, as well as after coronary angioplasty and stenting. They prevent fibrinogen binding and platelet aggregation.
Tirofiban, abciximab, eptifibatide
This is manifested by respiratory distress, pinkish sputum or frank hemoptysis, coarse rales, expiratory wheezes, tachycardia, S3 gallop, diaphoresis, AMS.
CHF with left ventricular failure
This is manifested by elevated central venous pressure, pedal edema, hepatomegaly, cyanosis, and sometimes pleural effusion or ascites. It is oftentimes seen in long-standing CHF.
CHF with right ventricular failure
Use of this medication leads to corneal epithealial whorl-like microdeposits in nearlly all patients who use it for an extended time. Patients may report hazy vision or colored halos around lights. Patients may also get discoloration of periocular skin (slat-gray or blue color) due to photosensitivity. Rarely, a patient may have associated optic neuropathy.
Amiodarone
These medications may cause a keratoconjunctivitis sicca-like syndrome likely due to decreased lacrimation. They may also decreased IOP and cause certain visual disturbances and visual hallucinations.
Systemic beta blockers
This medication causes glare and disturbances of color vision, including decreased vision; blue-yellow pattern defects; a yellow, green, blue, or red tinge to objects; and colored halos (mainly blue) around lights. They may also have yellow or green flickering vision, colored borders around objects, glare phenomena, light flashes, scintillating scotomata, frosted appearance to objects, and formed visual hallucinations.
Digoxin
These medications may cause angioedema involving the eye and orbit due to disruption of bradykinin metabolism.
ACE inhibitors
This is the ischemic, but not infarcted, area of the brain in a stroke. It is dynamic, and earlier treatment can prevent infarction and permanent neurologic injury.
Penumbra
This can present with the classic triad of Horner’s syndrome, neck pain/HA, and neurologic signs and symptoms.
Carotid dissection
These are the annual stroke rates among patients with isolated transient monocular visual loss (TMVL), retinal infarct, or retinal TIA, respectively. Untreated, these patients have a 30% risk of MI and 18% risk of death at 5 years.
2%, 3%, and 8%
85% of these develop in the anterior part of the circle of Willis, most commonly at the origin of the PCA from the internal carotid artery. Presentation: HA, CN 3 palsy involving the pupil.
Congenital saccular (or “berry”) aneurysms
This is a group of reversible, obstructive airway diseases in which the airways are hyperresponsive and develop an inflammatory response with bronchospasm to various stimuli.
Asthma
This is a group of irreversible obstructive airways diseases in which forced expiratory flow is reduced in either a constant or a slowly progressive manner over months to years.
Chronic obstructive pulmonary disease (COPD: emphysema, chronic bronchitis, peripheral airway disease)
This is a diverse group of conditions that cause diffuse parenchymal damage to the lung, leading to a reduction in total lung volume, diffusing capacity, and vital capacity. It can also occasionally be seen in patients with disease of the chest wall, respiratory muscles, pleura, or spine.
Restrictive lung disease (fibrotic disease, granulomatous disease, collagen vascular diseases, etc)
What FEV1/FVC ratio suggests obstructive lung disease?
<70%
What total lung capacity suggests restrictive lung disease?
<70%
These are three eye findings associated with OSA.
Floppy eyelid syndrome, keratoconus, and nonarteritic anterior ischemic optic neuropathy (NAION)
Nasal CPAP for OSA can worsen these two eye conditions.
Glaucoma (can moderately increase IOP), DES
These are three short-acting beta-2 agonists used to treat bronchoconstriction.
Fenoterol, salbutamol, isoetharine