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UAB SON Patho Exam 3
! AAA UAB SON Patho Exam 3 Review
| Question | Answer |
|---|---|
| 5 normal processes important to endocrine function | biological rhythm, blood pressure, fluid volume, metabolism & nutrient availability, and mineral control & electrolyte balance |
| mammary gland hormone | prolactin |
| thyroid gland hormone | TSH |
| adrenal gland hormone | ACTH (stress hormone) |
| gonads hormone | FSH/LH |
| hormone linked to growth of target cells | somatostatin |
| hormone linked to melanocytes | MSF (linked to cancer) |
| hormone in direct control of BP | adrenal epinephrine |
| hormone with indirect control of BP | norepinephrine |
| adrenal epinephrine stimulated by | sympathetic nervous system |
| 4 actions of epinephrine and norepinephrine on BP | MAP increased, increased Ca++ to heart cells, vasoconstriction of arteries in abdominal circulation w/ vasodilation of muscle, and relaxed bronchial smooth muscle to increase ventilated zones |
| long term control of fluid volume by | hypothalamus |
| hormones related to fluid volume | vasopressin and renin-angiotensin aldosterone system |
| hormone that causes water retention and is triggered by increase in CSF osmolarity | vasopressin |
| purpose of this system is to increase fluid osmolarity so water moves from cells to vessels and potassium is lost in the urine (affected by sodium) | renin-angiotensin-aldosterone system |
| 6 hormones involved in control of metabolism & nutrient availability | insulin & glucagon systems, neuropeptide-Y, leptin, cholecystokinin, adrenal hormones, thyroid hormones |
| control blood sugar and are major regulators of feeding and fasting states | insulin and glucagon systems |
| hormone from hypothalamus that primarily stimulates hunger | neuropeptide-Y |
| hormone that regulates fat storage | leptin |
| peptide hormone that stimulates digestion of fat and protein | cholecystokinin (CCK) |
| hormones of metabolism that increase with heat loss and decrease with heat gain | adrenal and thyroid hormones |
| 4 hormones involved in mineral control & electrolyte balance | aldosterone, vasopressin, calcitonin, parathyroid hormone |
| 2 hormones that affect sodium and potassium | aldosterone and vasopressin |
| hormone associated with calcium control, released when there is a high blood Ca++ to cause increased bone absorption of calcium | calcitonin |
| hormone associated with calcium control, when there is low blood Ca++ to cause absorption of calcium from bone | parathyroid hormone |
| 4 groupings of endocrine disorders | hyperendocrine, hypoendocrine, primary, and secondary |
| excessively high blood concentrations of a hormone | hyperendocrine |
| endocrine disorder caused by secreting tumors or excessive stimulation of the gland by trophic signals | hyperendocrine |
| excessively low blood concentrations of a hormone | hypoendocrine |
| endocrine disorder caused by failure or congenital absence of glandular tissue, surgical removal of the gland, or lack of normal trophic signals | hypoendocrine |
| direct malfunction of hormone producing gland | primary endocrine disorder |
| malfunction of hypothalamus/pituitary cells that control hormone producing gland | secondary endocrine disorder |
| endocrine disorder caused by intrinsic defects within the hormone secreting gland | primary endocrine disorder |
| endocrine disorder caused by abnormal pituitary secretion of trophic signals | secondary endocrine disorder |
| dysglycemia with impaired glucose tolerance (an intermediate between normal and diabetes) and impaired fasting | pre-diabetes |
| constellation of cardiometabolic risk factors including dyslipidemia, obesity, glucose intolerance, and hypertension; group of disorders with insulin resistance as a main feature | metabolic syndrome |
| disorder of glucose tolerance not diagnostic of diabetes characterized by fasting blood glucose value between 100 and 126 | impaired fasting glucose |
| disorder of glucose tolerance not diagnostic of diabetes characterized by 2 hour post-prandial blood glucose value between 140 and 200 | impaired glucose tolerance |
| an endocrine disorder characterized by impaired glucose entry into insulin sensitive cells due to an absolute or relative deficiency of insulin | diabetes mellitus |
| 8 signs of insulin resistance | acanthosis nigricans, skin tags, hirsutism, acne, menstrual irregularities, android appearance in women, virilization, male pattern vertex balding |
| Characterized by an absolute insulin deficiency caused by pancreatic cell failure; two forms include immune-mediated and idiopathic DM | type 1 diabetes mellitus |
| Beta-cells of the pancreas are destroyed, resulting in loss of insulin production. Immune mediated: Associated with certain HLA genetic makeup; may be autoimmune; viral infection or exposure to a toxic agent may be a responsible environmental influence. | immune-mediated T1DM |
| Associated with beta-cell destruction without autoimmune markers. | idiopathic T1DM |
| Characterized by a relative insulin deficiency caused by decreased tissue sensitivity and responsiveness to insulin; risk factors include aging, sedentary lifestyle, obesity, and genetic predisposition. | type 2 diabetes mellitus |
| caused by delayed meals or snacks, increased exercise or activity, alcohol intake without food, intensive insulin therapy, medication errors | hypoglycemia |
| symptoms include shaking, sweating, palpitations, hunger, slurred speech, mental confusion, disorientation, extreme fatigue, lethargy, seizure, unconsciousness | hypoglycemia |
| treatment includes ingestion of glucose or carbohydrate containing food | hypoglycemia |
| diabetic emergency most common in T1DM | diabetic ketoacidosis |
| diabetic emergency most common in T2DM | NKHHC |
| caused by hyperglycemia, sudden onset precipitated by infection, stress, inadequate insulin dose | diabetic ketoacidosis |
| symtpoms include hot and dry skin, dehydration, Kussmaul respirations, fruity or ETOH or acetone breath, blood glucose >250, positive ketones, polyuria, polydipsia, and polyphagia | diabetic ketoacidosis |
| treatment includes supplemental insulin, fluid and electrolyte replacement, and medical monitoring | diabetic ketoacidosis |
| caused by hyperglycemia, onset is gradual precipitated by infection, stress, or poor fluid intake | NKHHC |
| symptoms include profound diaphoresis and dehydration | NKHHC |
| treatment includes insulin and rapid IV fluid replacement | NKHHC |
| rebound hyperglycemia following an episode of hypoglycemia caused by counter regulatory hormone release (check blood glucose at 2am) | somogyi effect |
| A marked increase in insulin requirements between 6 am and 9 am as compared with the midnight to 6 am period. | dawn phenomenon |
| 3 macrovascular complications of diabetes | coronary artery disease, cerebrovascular disease, peripheral vascular disease |
| 3 microvascular complications of diabetes | retinopathy, nephropathy, neuropathy |
| 6 alterations in physiologic function associated with microvascular complications of diabetes | blindness, ESRD/CKD, foot ulcers, sexual dysfunction, infections, gastroparesis |
| aka gallstones, Chief complaint of most patients is biliary colic, a persistent epigastriac or right upper abdominal pain. A typical episode lasts several hours. Brought on by a meal or may occur at night. | cholelithiasis |
| refers to inflammation of the gallbladder wall. It is classified as acute or chronic, according to its clinical manifestations | cholecystitis |
| Characterized by severe right upper abdominal pain that may radiate to the back. Present in about 90% of patients. Bacterial infection may be present although it is not thought to be the direct cause. | acute cholecystitis |
| an important subgroup of acute cholecystitis. Tends to occur in the setting of major surgery, critical illness, trauma, or burn related in jury. Pts tend to be male and older than 50. | acalculous cholecystitis |
| inflammation of the gallbladder wall due to persistent low grade irritation from gallstones. Diabetes and obesity are important predisposing factors | chronic cholecystitis |
| most common causes are are hemolysis and ineffective erythropoises. The reabsorption of hematomas in patients with mild liver disease is a common cause of mild jaundice due to unconjugated hyperbilirubinemia. | prehepatic jaundice |
| dysfunction of each of the hepatic steps in bilirubin metabolism may cause this type of jaundice | hepatic jaundice |
| RNA virus that is spread by the fecal-oral route. There is a 2-7 week incubation period. May be asymptomatic or mildly symptomatic without jaundice. This is diagnosed through serologic testing. Presence of IgG indicates previous infection | hepatitis A |
| partially double stranded DNA virus, has an incubation period of 2-6 mos. Infection is longer and more insidious than HAV and may involve a variety of immune complex related phenomena, including urticaria, arthritis, serum sickness, and glomerulonephritis | hepatitis B |
| Single stranded RNA virus that belongs to the Flavivirus family. Worldwide about three percent of the population is chronically infected. Mode of transmission of closely resembles HBV, although sexual and perinatal transmission are much less likely. | hepatitis C |
| may coincide with or succeed HBV infection and requires its presence for replication. This disease is primarily transmitted by parenteral routes and by intimate personal contact | hepatitis D |
| may be the most common cause of acute hepatitis in the developing countries. Cases in developed countries are usually related to recent travel. An RNA virus spread via the fecal-oral route, especially through contaminated water | hepatitis E |
| a group of diseases characterized by inflammation of the liver that lasts six months or longer. The condition may be idiopathic, autoimmune, or metabolic. It may also follow acute viral hepatitis or may be caused by hepatotoxic drugs or toxins. | chronic hepatitis |
| often called triaditis. Chronic, low grade liver inflammation of any cause. Condition may be asymptomatic or may be associated with mild, nospecific symptoms. Progressive liver disease does not usally develop, and no drug treatment is indicated. | chronic persistent hepatitis |
| a PROGRESSIVE destructive inflammatory disease that extends beyond the portal triad to the hepatic lobule. Symptoms typical of acute hepatitis are often seen. Eventually chronic active hepatitis often culminates in cirrhosis and end stage liver disease | chronic active hepatitis |
| generally classified as hepatitis A, B, C, D, and E | acute viral hepatitis |
| also known as enteric, because it is generally transmitted by ingestion of contaminated substances. Flu-like symptoms are less severe than HBV symptoms. Early treatment with y-globulin and vaccination after exposure may be effective in preventing disease. | hepatitis A |
| known as Serum Hepatitis because its usually route of transmission is through infected blood. Incubation period is longer and the severity of symptoms (jaundice) greater than in HAV | hepatitis B |
| known as non A and non B. Resembles HBV in route of transmission. Develops in 85% of cases and is usually asymptomatic until advanced liver disease intervenes. Treatment is with intramuscular pegylated interferon and oral ribavirin for 6 -12 months. | hepatitis C |
| coinfects with HBV and requires the presence of HBV to be active | hepatitis C |
| Prevention of HBV infection also prevents | hepatitis D |
| common virus in the developing world that causes an illness similar to HAV but has a HIGH MORTALITY RATE in pregnant women | hepatitis E |
| characterized by persistent inflammation of the liver lasting six mornths or more. Automimmune disease, viral hepatitis, (B and C), toxins and metabolic disease may cause this, and it may progress to cirrhosis. | chronic active hepatitis |
| 6 major structures of the GI tract | Mouth, pharynx, esophagus, stomach, and small and large intestines |
| 5 accessory GI structures | salivary glands, the pancreas, and the biliary system. (liver, gallbladder, and bile ducts) |
| 4 general functions of the GI tract in providing nutrients for the body | motility, secretion of digestive juices, digestion of nutrients, and absorption of nutrients. |
| mostly in the form of triglcyerides but also include phospholipids, cholesterol, and fat soluble vitamins A, D, E, and K. Digestion occurs in the small intestine, where fats are emulsified by bile. | lipids |
| composed of amino acids, undergoes digestion in the small intestine includes sources from food and from enzymes, digestion begins in the stomach. | proteins |
| digestion is initiated by the mouth by salivary amylase. Pancreatic amylase continues this process in the small intestine. | complex carbs |
| black blood found in drainage or excreta, such as feces | melena |
| feces containing bright red blood | hematochezia |
| blood in vomitus | hematemesis |
| Inflammation of the stomach and intestines, which may occur on an acute or chronic basis and is commonly caused by viruses | gastroenteritis |
| A progressive and irreversible loss of renal function over months to years defined by glomerular filtration rate of <60ml/min for 3 months or more | chronic renal failure |
| leading cause of CRF | diabetes |
| 3 characteristics of CRF | tubular atrophy, glomerulosclerosis, interstitial fibrosis |
| Renal fx remains normal ________% of nephrons are damaged | 75-80% |
| stage of CRF characterized by Decreased renal reserve: <75% nephron loss. Clinical findings: no S&S, BUN and creatinine normal, may not be diagnosed | stage 1 CRF |
| stage of CRF characterized by renal insufficiency: 75-90% nephron loss. Clinical findings: polyuria, nocturia, slight elevation in BUN and creatinine, may be controlled by diet and meds | stage 2 CRF |
| stage of CRF characterized by 90% nephron loss. Clincial findings: azotemia, uremia, fluid and electrolyte abnormalities, renal osteodystrophy, dialysis or transplant necessary. Fluid volume overload develops, aka ESRD | stage 3 CRF |
| 3 reasons for obstructive urinary disease | anatomic abnormalities such as ureteral valves, strictures of the urethral meatus, and stenosis at the ureterovesical or ureteral pelvic junction |
| factors that predispose an individual to renal calculi | previous diagnosis, males, 20-40 y.o., hypercalciuria, supersaturation, abnormal pH, low urine volume |
| 2 primary functions of renal system | maintaining fluid and electrolyte homeostasis and ridding the body of water soluble wastes |
| amount of fluid filtered per hour by renal system | 7L |
| renal system alters amount and composition of urine in order to | maintain normal blood volume and electrolyte composition within the body |
| 2 endocrine functions of renal system | production of erythropoietin and vit. D |
| what determines the filtrate volume | net filtration pressure |
| what determines the filtrate concentration as being permeable or non-permeable | capillary permeability |
| permeable components in renal function | H2O, electrolytes, glucose, urea, creatinine, or drugs |
| non-permeable components in renal function | bld cells, platelets, plasma protein |
| 2 variables that can be adjusted to change the filtration rate | glomerular hydrostatic pressure and plasma osmolarity |
| reabsorbs 2/3 of the filtered water, electrolytes, HCO3, glucose, amino acids, and vitamins | proximal convoluted tube |
| actively reabsorbs Na, K, Cl to produce a hypoosmotic filtrate and a high interstitial osmolality | ascending loop of Henle |
| reabsorbs Na (due to Aldosterone), H2O (due to vasopressin), Cl, urea, and HCO3 (due to pH). It also secretes H and K, ammonia and PO4 | distal convoluted tube |
| reabsorbs water under the influence of ADH and secretes H and K | collecting tubule |
| endocrine control that increases water permeability and reabsorption in the last portion of the distal tubule and collecting tubule | ADH |
| endocrine control that stimulates bone marrow to produce and secrete RBC in response to tissue hypoxia | erythropoietin |
| endocrine control that converts Ca to the active form and reabsorption occurs in the intestine | vitamin D |
| endocrine control that inhibits Na absorption in the collecting ducts and increases urine formation | atrial natriureatic factor |
| used to determine the renal disease by the presence of urinary casts | urinalysis |
| used to determine how much of a substance can be cleared from the body by the kidneys per a given amount of time | serum creatinine clearance |
| freely filtered substance, as well as insulin, and neither are reabsorbed or secreted so you can compare both to any substance (X) to determine the renal handling of (X) | creatinine |
| If creatinine clearance = clearance rate (X) then | X is neither secreted nor absorbed |
| If creatinine clearance > clearance rate (X) then | X is reabsorbed |
| If creatinine clearance < clearance rate (X) then | X is secreted |
| Reflects glomerular filtration and urine concentrating capacity and is the end product of protein breakdown | blood urea nitrogen |
| BUN increases as GFR ________ | decreases |
| BUN is a better measurement of | ARF |
| 5 factors that affect BUN | dehydration, altered protein intake, protein catabolism, ARF, and CRF |
| a collection of symptoms caused by the glomerular disease. It is characterized by an increase of glomerular capillary wall permeability to serum proteins. The predominant abnormality is the loss of large amts of protein in the urine (>3.5g/d) | nephritic syndrome |
| causes a disturbance in the glomerular basement membrane | diabetic nephropathy |
| manifestations of nephritic syndrome | hypoprotienemia, hypoalbuminemia, edema, hyperlipidemia, and hypercoaguability |
| inflammation of the glomerulus caused by immunologic abnormalities, ischemia, drugs, and toxins. Most common cause of ESRD. The epithelial layer of the glomerulus membrane is disturbed with loss of negative charges and change in membrane permeability | glomerulonephritis |
| 2 pathos of glomerulonephritis | 1) Deposition of circulating antigen-antibody complexes and formation of antibodies specific to glomerular membrane and 2) Activation of biochemical mediators of inflammation, altered membrane permeability and other alterations |
| 2 manifestations of glomerulonephritis | Hematuria (smokey brown-tinged urine and RBC casts) and Protienuria (exceeding 3-5g/d and primarily albumin) |
| a sudden, severe decrease in renal fxn that is potentially reversible. Associated with a decrease in GFR, oliguria (<500ml/d), and azotemia. | acute renal failure |
| Abrupt reduction in renal fxn with an elevation of BUN and creatinine levels | acute renal failure |
| decrease bld flow to kidneys leading to ischemia and necrosis | pre-renal failure |
| etiology of Pre-RF | Shock, CHF, pulmonary embolism, anaphylaxis, sepsis, and pericardial tamponade |
| obstruction of the urinary collecting system anywhere from the calyces to the urethral meatus | post-renal failure |
| etiology of Post-RF | urethral/bladder cancer, renal calculi, prostatic hyperplasia or cancer, cervical cancer, or urethral stricture |
| acute tissue damage to the kidney | intra-renal failure |
| etiology of intra-RF | nephritis, toxins, glomerulonephritis, vasculitis, ATN, renal artery or vein stenosis |
| phase of ARF that begins within 1day of hypotensive events, lasts 1-3weeks (varies with duration of ischemia or severity of injury), urine output may vary 10-20% is nonoliguric (<500mg/d), BUN and creatinine concentrations increase. | oliguric phase |
| phase of ARF with prompt onset with urine flow increasing rapidly, urine output up to 10L/d, electrolyte losses, BUN starts to fall, usually lasts 2-3weeks, and tubular fxn resumes | diuretic phase |
| phase of ARF where client begins to return to normal activity but the kidney fxn may not return to normal | recovery phase |
| – progressive loss over months to years. GFR <60ml/min. Advancement can sometimes be slowed, but it is ultimately irreversible and terminates into end-stage renal disease (ESRD) | chronic renal failure |
| leading cause of CRF | diabetes |
| secondary causes of CRF | acute tubular necrosis (from unresolved ARF), developmental/congenital conditions, cystic disorders, neoplasms, infections, or systemic conditions |
| stage of CRF- decreased renal reserve, serum creatinine and Bun are normal | stage 1 CRF |
| stage of CRF- renal insufficiency and more than 75% of kidney fxn is lost | stage 2 CRF |
| stage of CRF that includes ESRD | stage 3 CRF |
| when < 10% of renal fxn is left | ESRD |
| 5 types of STD "drips" | GC, chlamydia, trichemonas, BV, yeast |
| STD sore >1cm and painful | chancroid |
| STD sore <1cm and not painful | primary syphilis |
| STD sore- multiple lesions and painful | HSV-2 |
| accumulation of urine in the ureter | hydroureter |
| accumulation of urine in renal collecting system | hydronephrosis |
| 6 consequences of urinary tract obstruction | hydroureter, hydronephrosis, decreased GFR, postobstructive diuresis, infection, and renal failure |
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