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Pathophys-2 Final
Male & Female Repro, Endocrine, Nervous System, Dermatology
| Question | Answer |
|---|---|
| Cause(s) of primary parathyroidism? | Most common cause is parathyroid adenoma |
| Cause(s) of secondary parathyroidism? | Most common cause is renal failure (increased serum phosphate levels depress serum calcium levels (b/c PTH responds to both signals?), and this chronic hypocalcemia sends parathyroid into overdrive-- and (somehwo) you end up with HYPERCALCEMIA!) |
| What are the consequences of hypercalcemia in hyperparathyroidism? | Calcification (calcium phosphate) of soft tissue, hypercalciurira/renal stones, heart contraction abnormalities, muscle weakness |
| What are the manifestations of hyperparathyroidism? | (mostly from the hypercalcemia?) Stones (KD), bones (brown tumors and fracture from osteoclasis), moans (not sure why), groans (stomach ulcers- not sure why) |
| What are the causes of hypoparathyroidism? | Most commonly accidental removed of parathyroid during thyroidectomy. Could also be developmental disorder or autoimmune. Chvostek and Trousseau are the dx tests. |
| What are the manifestations of hypoparathyroidism? | Hypocalcemia, TETANY (no calcium to release muscle fiber contractions), carpo-pedal spasm, distal tingling, mood swings, arrhthymia, neuromuscular "irritability" |
| What are the causes of hyperaldosteronism? | Hyperplasia or tumor of adrenal cortex (adrenalcorticoid hyperplasia, adenoma) |
| What are the manifestations of hyperaldosteronism? | Elevated Na+, decreased K+, HTN (hyperaldosteronism is called Conn's disease) |
| What are the causes of Cushing‘s syndrome? | Cushing´s DISEASE is caused by excess cortisol (via ACTH) d/t pituitary tumor (adenoma). Cushing´s SYNDROME includes other causes: adrenal tumor, ectopic production of adrenocorticotropic hormone (ACTH) (aka corticotropin) by small cell lung carcinoma. |
| What are the manifestations of Cushing‘s syndrome? | moon face, buffalo hump, muscle wasting, osteoporosis, perhaps obesity |
| What are the causes of adrenogenital syndrome (aka congenital adrenal hyperplasia) in males? | congenital deficiency of enzyme necessary for synthesis of cortisol which results in excess production of ACTH and consequently excessd production of adrenal androgens |
| What are the manifestations of adrenogenital syndrome (aka congenital adrenal hyperplasia) in males? | Huge penis |
| What are the causes of adrenogenital syndrome (aka congenital adrenal hyperplasia) in females? | congenital deficiency of enzyme necessary for synthesis of cortisol which results in excess production of ACTH and consequently excessd production of adrenal androgens |
| What are the manifestations of adrenogenital syndrome (aka congenital adrenal hyperplasia) in females? | "Ambiguous genitalia" with freakishly enlarged clitoris and possibly fused labia and/or urogenital sinus (whatever that is) |
| What are the causes of Addison’s disease? | Most common cause is auto-antibodies. Prior to 1950s was TB. Could also be (bilateral metastasis to adrenal glands), "amyloidosis" |
| What are the manifestations of Addison’s disease? | "Addled" by fatique, nausea/diarrhea, weight loss, hypotension, syncope, hyperpigmentation of skin ("fadded pig") |
| COMPARE AND CONTRAST neuroblastoma and pheochromocytoma (!!??) | Neuroblastoma is in kids ("blast") and often malignant. Pheochromocytoma in adults (dx´d by "vanilla" acid in urine: VMA) and mostly benign. Both include HTN symptoms, but seems like adult is more "paroxysmal" |
| CLASSIFY diabetes mellitus. (!!??) | Duh |
| What is the pathogenesis of hyperglycemia in diabetes mellitus type 1? | Islet cell (beta cell?) insufficiency and subsequent inadequate insulin production |
| What are the metabolic abnormalities contributing to hyperglycemia in type 2 diabetes? | "impaired beta cell FUNCTION" (??) |
| What are the risk factors for gestational diabetes mellitus? | BIG mother, BIG baby, BIG age, BIG number of previous births, h/o miscarriage, family history, prev preg w/ fetal abnormalities |
| What is the pathogenesis of polydipsia, polyphagia, and polyuria in diabetes mellitus? | Too much sugar in blood tells KD to pee, pee, pee. That results in dehydration/thirst. The "big appetite" comes from "abnormal utilization of protein/carbs/fats." |
| What are the 3 acute complications of diabetes mellitus? | DKA (ketoacidosis, mostly in Type 1). HHS (hyperosmolarity hyperglycemis state (mostly in Type 2). And.... strangely enough: HYPOGLYCEMIA (!!??) |
| What is the pathogenesis of diabetic ketoacidosis? | Liver is breaking down triglycerides for fuel. By-products of this "lipolysis" is fatty acids and GLYCEROL. By-product of this (I think?) is KETONES!! Which are relatively acidic. (Blood can tolerate only very narrow range of pH.) |
| COMPARE the characteristics of DKA and hyperosmolar hyperglycemic state. (!!??) | DKA: ketonemia, kentonuria, glucose >250, bicarb <15, pH<7.3. HHS: blood glucose is over twice as high!! (>600), plasma osmolarity >310. DEHYDRATION (from the hyperosmolarity surely) |
| What are the macrovascular complications of diabetes mellitus? | Mostly accelerated atherosclerosis and its sequelae: MI, stroke, Gangrene (peripheral vascular disease) |
| What are the microvascular complications of diabetes mellitus? | "Thickening of basement membrane" of both vascular and nonvascular structures (glomeruli, tubules of KD) leads to problems of KD (glomerulosclerosis, pyelonephritis), EYE (retinopathy, cataracts, glaucoma), NERVES (neuropathies) |
| What is the pathogenesis of retinopathy? | "Microangiopathy" of retina leads to microaneurysm, hemorrhage and ischemia/infarct of retina |
| What are the pathologic changes in diabetic peripheral neuropathy? | Also microangiopathy: thickening/sclerosis of nutrient vessels to nerve leads to ischemia. (There are both somatic and autonomic (vasomotor--> postural HTN, GI, genitourinary, brain) neuropathies.) |
| What are the causes of ischemic stroke? | Duh ("interruption of blood flow in/to cerebral vessel") |
| What is the most common cause of ischemic stroke? | Thrombus in atherosclerotic vessel |
| What are the causes of hemorrhagic stroke? | (bleeding into brain tissue usually from a BV rupture d/t) HTN, aneurysm, arteriovenous malformation |
| What are the risk factors for stroke? | (think Todd English): smoking, HTN, hyperlipidemia, cocaine, male sex, advanced age, DM, obesity, OC use, elevated homocysteine levels |
| What is the difference between Wernicke and Broca aphasia? | Wernicke's is "wordy, words do not make sense" Broca's is "broken" (unable to form words BUT CAN UNDERSTAND!!) WT/BF |
| What are the manifestations of acute stroke? | Sudden onset neuro complaints: weakness, sensory abnormalities, vision changes, langage defect, "altered mentation" (HYPERREFLEXIA in both anterior and posterior circulatory involvement) |
| What are the manifestations of post-infarct cerebral edema? | PROJECTILE VOMITING (!!) 2-4 days later, "decreased consciousness," pupillary changes |
| What is the difference between Transient Ischemic Event (TIE) and stroke? | TIA symptoms resolve within 24 hours (typically withing 1-2 hours) |
| What is an intracranial aneurysm? | AAbnormal bulge or ballooning of a BV supplying the CEREBRUM (typically at arterial bifurcations) |
| What diseases are associated with intracranial aneurysm? | polycystic KD disease, coarctation of the aorta (both would increase arterial pressure) |
| What are the risk factors for intracranial aneurysm? | HTN, smoking, hypercholesterolemia (think Ian?) |
| What are the possible complications of intracranial aneurysm? | can rupture and bleed into SUBARACHNOID SPACE (seizure and HA are first sx. need CT scan ASAP!) |
| What is the etiology and pathology of arteriovenous malformation? | Congenital. Arteries/arterioles feed DIRECTLY into venous blood (venules/veins) without the nice capillary network that would typically buffer the differences in pressure. The venous channels are thus exposed to higher than normal levels of pressure. |
| What is the pathology of MS? | immune medicated inflammatory disease that attacks myelinated axons of the CNS |
| What are the manifestations of MS? | weakness of lower extremities, pins & needles sensory disturbances, diplopia or blurred vision or vision loss, urinary sphincter disturbances, gait impairment or clumsiness of upper extremities. Could also be vertigo, slurred speech, sexual impairment |
| What are the dx tests for MS? | MRI (brain/spinal cord) |
| What is Parkinson's disease? | idopathic, slowly progressive degenerative CNS disorder characterized by slow and decreased movement, muscular rigidity, resting tremor, postural instability |
| What is the pathophysiology of Parkinson's disease? | Loss of pigmented neurons of the SUBSTANTIA NIGRA (and other brain stem) dopaminergic cell groups (and thus depleted dopamine in these areas) |
| What are the manifestations of Parkinson's disease? | resting tremor, cog-wheel rigidity, bradykinesia, shuffling gait, mask-like face, c/b dementia |
| What is the difference between DELIRIUM and DEMENTIA with regard to: course? | dementia is generally progressive (delirium is typically sudden onset and either spontaneous resolution or waxing/waning, often more evident in evening) |
| What is the difference between DELIRIUM and DEMENTIA with regard to: reversibility? | (see above) |
| What is the difference between DELIRIUM and DEMENTIA with regard to: circadian variation? | delirium often more common after sundown |
| What is the difference between DELIRIUM and DEMENTIA with regard to: consciousness? | delirium includes altered consciousness |
| What is the difference between DELIRIUM and DEMENTIA with regard to: hallucination? | delirium |
| What is the difference between DELIRIUM and DEMENTIA with regard to: tremor? | delirium ("asterixis") |
| What is the difference between DELIRIUM and DEMENTIA with regard to: causes? | dementia thot d/t Alzheimer's, Pick's, multi-infarct, ETOH, tumor, B12 deficiency. delirium usually systemic infection, neoplasm, narcotic or benzo use, stroke, electrolyte imbalance, hyper/hypoglycemia, heart disease |
| What is the pathophysiology of Alzheimer's disease? | loss of neurons and synapses in cerebral cortex and some subcorticoid regions |
| What are the clinical features of Alzheimer's disease? | k |
| What is the best screening test for Alzheimer's disease? | k |
| What is the best diagnostic test for Alzheimer's disease? | short-term memory test (also "formal mental state examination") |
| Quick reality check. Give me 2 men's names for Adrenocorticoid HYPERfunction and 2 for HYPOfunction. | Conn's= too much aldosterone (HTN, high Na+). Cushing's= too much ACTH. Addison's is TOO LITTLE ACTH (d/t autoimmune, TB, tumors, amyloidosis). Think "Addled" by fatique, wt loss, diarrhea, low BP, fainting, infections, "fadded" pig: hyperpigmentation. |
Created by:
mrbarr
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