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338 Cards in this Set
- Front
- Back
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how to calculate osmolarity
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2 (Na) + BUN/2,8 + glucose/18
300 is normal (275-295) |
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zonula occludens
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tight junction between cells; can be tight or leaky
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alcohol does what to cells
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hydrophobic diurectic lose sodium and water creating hypertonicish solution and lose some from ICF too to shrink cells; plasm osm stays about the same
hang over---dehyrated cells need to drink fluid to rehydrate |
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primary renal insufficiency does what to cell osm
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no aldosterone to retain salt so lose salt and water; to balance out ICF gains fluid so both compartments also lose plasma osm
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sodium and potassium naturally ICF/ECF vs Na/K pump
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Na likes intracellular/K extra ; 3Na outside/2 K inside cell w/ pump
ICF- major cation K and Mg and protein ATP ECF-1/3, NA w/ Cl and bicarb; very little protein insterstitially the most of major plasma protein are albumin and lgublins 60/40/20 |
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induce/inhibit P450
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P-450 interactions Inducers (+)
Quinidine", Barbiturales, St, john's wort, Phenytoin, and rifampin, Griseofulvin, Carbamazepine Chronic alcohol use Inhibitors (-)--Sulfouamides, Isoniazid, Cimclidine, Ketoconazole Erythromycin, Grapefruil juice Acute alcohol use Inducers: Queen Barb Steals Phen-phen and Refuses Greasy Carbs Chronically. Inhihilors: Inhibil yourself from drinking beer from a KEG because il makes vou Acutdv SICk. |
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renal clearance equation
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C=UV/P
clearance of X mL/min =urine conc x urine flow rate / plasma concentration |
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renal clearance <GFR/ >GFR =
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net tubular reabsorption if <GFR=resorption measure urea?
if >GFR=secretin measure PAH? C=UV/P |
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filtration fraction
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GFR/RPF normal is .2
GFR est w/ creatinine (overest) RPF estimated w/ PAH (underest) |
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what constricts the efferect arteriole in kidney?
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angiotensin 2 (DM)--dec RPF inc GFR inc FF
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what constricts the aff arteriole in kidney?
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sympathetics (no change in FF, dec GFR and RPF)
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stone in ureter affects GFR/RPF how?
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dec GFR, no change in RPF and dec FF
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2 things that can decreases SaO2 without Pao2 decreasing
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Methemoglobinemia
carbon monoxide poisoning |
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A-a gradient equation
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A-a %O2 (.21) x 713 - Pco2/.8
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stool osmotic gap
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300- 2 (Na + K) >100 is osmotic; secretory <50
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head and neck SNS
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T1-4
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heart SNS
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t1-5
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lungs SNS
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T2-7
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esophagus SNS
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t2-8
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upper gi nerves
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t5-9, greater splanchinic and celiac ganglion
===stomach liver GB spleen pancreas and dodenom vagus nerve para before lig of tretz |
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midle GI nerves
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T10-11 lesser splanchinic supper mesenteric ganglion
pancreas duodenom, jejunum, ilium, asending colon, proximal 2/3 of transverse colon vagus para |
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lower GI nerves
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T12-L2 least splanchinic nerve; inf mesenteric ganglion
distal 1/3 transverse colon, desceding colon and sigmoid, rectum pelvic splanchic para |
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appendix SNS
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t12
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kidneys sns
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t10-11
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adrenal medulla sns
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t10
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upper ureters sns
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t10-11
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lower ureters sns
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t12-L1
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bladder t11-L2 sns
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T11-L2
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gonads sns
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t10-11
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uterus and cervix sns
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t10-l2
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erectile tissue of penis and clitorus sns
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t11-l2
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prostate sns
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t12-l2
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arms sns
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t2-8
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legs sns
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t11-l2
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small intestine pns
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vagus
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large intestine ascending and transverse pns
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vagus
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distal half of large intesting after splenic flexure pns
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pelvic splanchinis
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kidneys an dupper ureter pns
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vagus
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lower ureter and bladder pns
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pelvic splanchnics
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ovaries and testes pns
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vagus
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reproductive structures like prostate uterus, cervics, penis pns
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pelvic splanchnics
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L3-5???
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nothing!!!
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pupils ANS
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para: contstrict miosis
dilates (mydriasis |
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lens ANS
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contracts for near vision parasymp
sligh relax for far vsion symp |
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glands (nasal, lacrimal parotid, submandib, gastric pancreatic )
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stim copious sec para; symp VC less sec
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sweat glands ANS
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para--sweat on palsm of hands
symp--copious sweat cholinergic |
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heart ANS
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para-dec contractility and conduction velocity; symp--inc contractility and conduciton velocity
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lungs ANS
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brochiolar sm--contracts in para, relaxes in smp
resp epithelium--dec goblet cells to enhance secretions para; inc goblem thick secretions |
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GI ANS
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sm in lumen--contracts in para, relaxes in symp
sphincters--relax in para, contracts in symp secretion and mitiliy--inc para, dec symp |
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systemic arterioles ANS
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skin and viseral vessels contract in symp
sk mm--relaxes in symp |
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GU ANS
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bladder wall detrusor--cotnracts in para, relaxes in symp
bladder sphincter trigone relaxes in para; contracts in in symp penis--erect in para; ejaculation in symp pee in parasymp |
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kidneys ANS
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symp--VC of aff arteriole; dec GFR dec urine volume
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ureters ANS
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normal peristalsis in para; rterospasm in symp
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liver ANS
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sligh glycogen synthesis in para; glycogenolysis release of glucose into blodd in symp
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uterus ANS
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body--relax para, constrcits symp
cervix; constricts para, relaxses symp |
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peripheral receptors
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sn to Po2 arotic/carotid body
----high altitude receptor to inc breathing |
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medullary receptors
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resp center sn to H+ ions acid
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most hypoxic hepatocytes and name towards heart
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zone 3--central vein (term hepatic venule)-->hepatic vein-->IVC
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hypoxia in the heart, kidney, liver
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subendocardium (angina in CAD, ST depression), central vein, TAL and proximal tubule
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drug metabolism P450
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adrenal, liver and SER
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why do women get drug easier?
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alcohol DH metabolize
we have inadequate alcohol DH in stomach and SI only in liver more cirrhosis **also native americans |
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lysosomes have
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MPO, peroxides ect
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what makes the enzymes for lysosomes?
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RER-->post translational modification in golgi it is a stamp to tell where to go
MANNOSE -->lysosome I cell disease missing mannose |
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I cell disease
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missing mannose; inclusinn cell
golgi failed def of phosotransferase random rlesease; psycomotor retardation and early death nothing in lysosomes **opp is chediak higashi |
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chediak higashi
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membrane protein fusion defect
lysosomes don't fuse w/ phagosomes AR; giant lysosomes (never emptied) red ; bacteriocidal defect; MT defect opp is I cell disease b/c nothing inside whereas this has tons inside |
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mallory body
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ubiquiton; intermediate filaments
marked for destruction by proteosomes ***aldehyde in alcoholic liver disease damages keratin IF in the liver |
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lewy body
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uibiquiton; intermediate filaments
marked for destruction by proteosomes parkinson's disease--neurfilaments MPTP---fries the brains get parkinson's |
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MCC of fatty liver
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alcohol
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explain fatty change in liver
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alcohol DHAP-->G3P-->TG
VLDL NADH forces pyruvate to become lactase (LA) so fasting hypoglycemia not enough to make ATP acetyl coA-->make FA via palmitic acid and ketone bodies acetyl acetyl coa-->BOHB inc FA and ketone bodies DHAP-->glycerol 3p -->TG--VLDL + apo B100 (keeps it soluble in water) DHAP usually does glycoslysis pathway inc hydrolysis of adipose, inc synthesis, dec B-ox B-ox of FA dec (in mitochondira) |
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triglyceride liver makes what fat?
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VLDL
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what fat do you ingest? TG
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chylomicrons
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B-oxidation located in the ?
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mitochondria
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B48 transports?
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CM packages and helps secretion into blood stream
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B100 transports?
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VLDL and packages and helps secretion into blood stream
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not enough proteins ingested and inc carbs
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kwashishocor fatty liver can't transport it out no apoporteins---apethetic
ascities (dec oncotic pressures)--voracious hunger |
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where is ferritin stored?
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in macrophages mostly and liver
ferritin (soluble) stores iron degrades into hemociderin in liver; heme system is P450 and porphyrins |
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aortic valve stenosis hear where?
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2nd intercostal space on the right
midsystolic murmur radiating to the neck causes LVH and progressive pulmonary congestion. harsh systolic murmur diamond shpaed opening click and radiation along arotic arch so audible in the left cervical region bicuspid valve calcification 4th decade. later decades 6thish calcified in old age |
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chronic pancreatitis
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exocrine--dysfunction malaboroption
endocrine--B islet cells gone diabetes type 1 calcification; MCC alcohol; dystrophic calc |
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atherosclerosis
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calcified dystrophic calc
atrophy cerebral MCC |
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calcified in brain by?
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basal ganglia toxi
pineal gland older patients CMV-periventricular |
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nephrocalcinosis
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clacified metastatic; in the collecting tubule in basement membranes
---inc serum calcium or phosphorus POLYURIA---inc calcium-->due to nephrogenic diabetes insipidus, renal failure ADH in collecting tubules |
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name 3 stem cells that are labile
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skin, marrow, GI tract
why chemo suppressive agents have diarrhea and bm suppression |
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hypertrophy of LV MCC
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essential hypertension due to AL
sarcomeres in parallel determine how duplicate via genes |
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hypertorphy and dilated of LV due to?
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preload inc; sarcomeres in series
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prostate hyperplasia hormone
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dihydrotestosterone around urethra
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hypertrophy of thyroid due to?
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graves disease Ab against TSH
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prostate hyperplasia causes?
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bladder hypertrophy
MCC of diverticula in bladder |
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normal gynecomastia in males?
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newborn, adolescent, elderly
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smoking causes what in bronchus what metaplasia?
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from ciliated pseudostratified glandular epithelium-->squamous dysplasia
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gross vs microscopic inarct
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infarct (pale vs hemorragic) vs coagulation necrosis
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small bowel infarction presentation
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hemorragic, step ladder fluid b/c not movement air and fluid, bloody diarrhea, diffuse abdominal pain, ileus (no bowel sounds) no peristalsis-->ruptures peritonitis rebound tendititis
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a fib
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embolus esp to renal artery-->sudden onset of flank pain and hematuria
lose a wave |
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polyarteritis nodosa
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vascultitis; embolism to renal-->infart
assoc w/ hep B assoc w/ nodules-->aneurysms weakening of wall of vessel |
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what causes wet gangrene?
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clostridium perfringens, gas and bubble---myonecrosis
also B fragilis liquefactive necrosis anaerobic |
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C. tetanae NTs
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glyceine and GABA
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2 things causes caeseous necrosis
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TB and systemic mycoses---lipids from cell wall
T4HS multinucleated giant cells |
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enzymatic fat necrosis assoc w/
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breasts and pancreatitis--soap formation (ca + FA) lipase
MUST CT PANCREAS |
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best test for looking at pancreas
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CT b/c it's retroperitoneal
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enzymes elevated in pancreatitis
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amylase (goes down after 4 days nad is present in the urine) and lipase (more sp for pancreas)
inc GFR around 3/4 days so filtures amylase pain radiates to back; localized ileus=sentinal loop due to inflammatory lesion |
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sentinal loop
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localized to ileus=sentinal loop due to inflammatory lesion
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what hormone makes a female fetus into a male?
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Mullarian inhibitory factor
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TNFa
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wasting disease in cancer
apoptosis caspases activated |
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signals modulators of apoptosis (2)
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BCL-2 prevents apoptosis (antiapoptosis)---holds onto cytochorme C
TP53 suppressor gene (apoptosis gene)--->repair cell in G1 phase if not act BAX gene-->apoptosis caspases group for apoptosis-->proteases and endonucleases; NO PHOSPHOLIPASES; cell membrane intact all the way to the end |
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pressure ulcers
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in DM--neuropathy can't feel bottom of feet
osmotic damage--burning foot symdrome, lose axons peripherally ischemia not the main reason for it |
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T1HS
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IgE mediate release of histamine from mast cells
ACUTE INFLAMMATION IS NOT IGE MEDIATED NOT T1HS |
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tumor (swelling)
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caused by histamine; venular permeability
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dolor
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PGE2 and bradykinin
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neutrophil events
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rouleux from fibrinogen pushed to side margination-->sticky selectins (ICAM VCAM) on neutrophil and endothelial cell to roll-->sticking and find hole-->has collagenase to transmigrate out (cancer does that too)-->rbcs/lymphocytes can move out-->exudate
C5a LTB4--activating adhesion molecules on neutrophils Il-1 and TNF activtion--on endothelial surface B integrins--CD11/18 glue for neutrophils **plt glue is vWF |
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B integrins
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CD11/18 act by C58 and LTB4
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newborn cord is still attached
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LAD1--due to selectins mild
LAD2--CD11/18 integrins bad problems wound healing |
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opsonins
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IgG and C3b
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monocytes opsonins
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C3b IgG RBC macrophages removal in spleen-->extravascular hemolysis-->hemolyzed UCB-->jaundice
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3 diseases can't opsonize
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chediak higashi, bruton's, common immunodeficiency SCID
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MPO system
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NADPH oxidase -->respiratory burst test NBT test, chemimmunescence test
NADPH made in PPP; missing in G6PD deficiency-->infection and hemolysis from drugs sulfa drugs/nitro drugs CGD missing NADPH oxidase superoxide-->SOD +H2O2--> MPO def--AR, no bleach; CGD--XR, no burst |
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catalase + means what?
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staph knocks of H2O2 so neg resp burst in CGD
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chemotaxis agents
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C5a LTB4
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NO
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VD of arterioles; endothelial and mac
septic shock FR gas |
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IL-1 TNF
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fever, stim hypothalamus PGE2
Acute phase reactants in liver leukocytosis activated complement hepcidin |
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bradykinin
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pain VD inc vessel permeability
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PGE2***
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VD--renal aff arteriole, fever, dolor pain
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prostacyclin
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Vd; prevent plt aggregation; not affect by NSAIDs
PGI2 |
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C5a
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CD11/18 act and chemotaxis
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what activates PLA2
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calcium
inhibited by corticosteroids |
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precursor prostaglandin
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PGH2
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aspirin affects what?
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TXA2 on plt
PGI2 prostacyclin--no affects b/c on endothelial cells |
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chronic inflammation
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moncytes (open chromatin pattern), fibrosis and scarring
not much exudate; IgG acute IgM ie TB, lupus |
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plasma cells
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lots of RER make antibody; like a fingerprint; nucleus to periphery
non in brutons pre-B-->B SCID B-->plasma |
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granuloma inflammation
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T4HS class 2 T helper cells and macrophages release-->IL-2 night sweats and Il-12--- makes memory T cells
T help releases IFN gamma act macs to kill; MIF (makes macs stick together) becomes epitheloid cells --multinucleated giants cells dead cell tombstone T4HS delayed type NOT antibodies; if CD8 kills cancer ect TNF also involved |
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IL12
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from mac memory T cells
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T4HS
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delated type hypersensity in granuloas
CD8 T cell can kill cancer ect |
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PPD
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langerhans histiocyte CD1 burbick granules
angigen processory of skin presents to memory T cells releases cytokines and measure tumor immunocomp--5mm; hospital--10; normal--15 |
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supporative inflammation
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see on surface liquefactive
appendicitis see on outside |
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hyaluronidase
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spreading factor; cellulitis erysipilas
strep A |
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diptheria inhbits
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B ox of FA in heart; toxic myocarditis MCCD
EF-2 |
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how is C diff spread
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in hospital spores
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how to treat C diff
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metronidazole NOT vancomycin (causes resistance)
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how to test for C diff
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cytotoxin assay in stool
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secondary intention healing
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infected wound leave open; myofibroblasts impt
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healing primary intention
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clean wound and oppose
crosslinks hydroxylation anchor for crosslinks 3a chains tropo collagen tensile strength -->hydrox by vit C and copper lysl oxidenase cross linking-->2 wks type 3 collagen-->remodeling type 1 collagen via collagenase (zinc) to help replace |
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key for wound healing
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granulation tissue-->scar
fibronectin chemotactin to make granulation tissue ---pyogenic granuloma |
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3 things needed in wound healing
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vit C--hydroxylation (proline and lysine)-->perifollicular hemorrhages
copper--cross link lysyl oxidase zinc--collagenase remodeling |
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collagen defect syndrome
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EDS
-MVP, aortic dissection |
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fibrillin loss
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MVP, aortic dissection, arachnodactaly, dislocated lenes, spider finders
--marfans |
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CNS repair
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astrocytes (like fibrocytes), microbial cells (like macs)-->gliosis
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T1 collagen
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ones tendons scar tissue
bone (one) |
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type 3 collagen
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early wound repair
Reticulin, skin, bv, uterus, fetal tissue, granulation tissue |
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type 4 collagen
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basement membrane
under the FLOOR (four) |
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type 10 collagen
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epphyeseal plate
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rouleu caused by
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SED rate--ESR, anemia, polycythemia,
fibrinogen dec rouleaux-- |
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CRP
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indicator acute inflammation
awesome tests CAD disease---inflammatory plaques premature rupture of membranes in pregnancy --if elevated then put on a statin get LDL down to 70 to dec atherosclerosis ***also homocystine inc risk of thrombosis (note that folate/B12 inc it too) |
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protein electrophoresis
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albumin migrates fast more neg charges all COO-; more acidic (aspartate, glutamate); attracts Ca+ :)
put in alkaline environment more Coo- less COOH??? Ig more basic; AA used to synthesze APRs chonic inflammation dec albumin but in IgG!!! polyclonal gammopathy; always bening not a spike for neoplastic albumin>a1 anatrypsin |
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CLL have what cells?
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inc B cells but can't transform to plasma cells
hypogammaglobulinemmia??!?!? can die of infection |
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corticosteroids do what?
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neutrophilic leukocytosis--dec activation of neutrophil adhesion molecules (selectin/integrins inact); lymphopenia--apoptosis of B/T cells-->less immunoglobulins and no CMI; eosinopenia--apoptosis
inact PLA2--no LT or PGs --dec collagen synthesis--less scar tissue (surgeons give) --meningeal disease give prevent fibrosing arachnoid granulations (w/ steroids) |
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what produces fibrinogen?
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IL-1 TNFa
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acute or chronic inflammation which causes necrosis
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acute
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TNF activates?
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neutrophils/macs/endothelial cells
activates -->caspases-->proteases and endonucleases-->apoptotic bodies |
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when glucose goes into a cell it?
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gets phosphorylated
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what are located in ECF/ICF
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Na, Cl, glucose
K urea freely difuses |
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serum Na calculated by?
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TBNa/TBW
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diastolic murmur beginning with a snap
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mitral valve stenosis
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machinery murmur
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PDA; shunting of blood aortic and pulmonary
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midsystolic click
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MVP
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3 causes of hypertonic loss of Na
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diuretics MCC; addison's; 21-Hase deficiency (salt loser)
will be super try but will have swelling of cells-->edema |
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causes of hyponatremia gain pure water
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siADH, chloropropnanide
no physical signs no pittign tx: restrict water; lasix-->then do hypertonic saline get them close to normal range but not in it |
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hypotonic gain of Na
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edema states
RHF MCC, cirrhosis, nephrotic syndrome RHF-->dec CO-->kidney not getting enough, ADH distended carotid arteries, inc hydrostatic pressure; dec EABV |
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hypotonic loss of Na
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osmotic diuresis glucose and mannitol; sweat
dry skin, skin turgor positive tilt test ---sports drinks have sodium, glucose |
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hypertonic loss of water
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diabetes insipidus; insensible water loss in fever
PE is normal |
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hypertonic gain of Na
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antibiotics w/ Na, excessive sodium bicarbonate (treat metabolic acidosis but rarely)
--pitting edema |
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hyperglycemia in osmotic
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inc Posm; dec serum Na
high glucose in ECF, water moves to ECF so hyponatremia to Na |
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resp alkalosis
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<33 Co2; acute >18, chronic bicarb is 12-18
s/s--tetany (carpal tunnel spasm, COO-), light-headedness, CNS stim--anxiety, pregnanyc, salicylate poisoning lung disease asthma early phase, restirctive lung disease, pulmonary embolus |
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resp acidosis
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>45
acute bicarb <,30; chronic >30 --somnolence-->coma, cerebral edema (vasodilate leak) ---CNS depression trauma, barbituaties --upper airway obstruction:epiglottitis, croup --chest bellows dysfuction: paralysis mm (polio, ALS, GBS) lung disease--COPD, ARD, pulm edema, severe asthma (tired of breathing) --hypoK, hypoP lower ATP paralysis of mm in lungs (VC) |
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increase AG acidosis
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inc lactate, salicylate , BOHB ACAC;adding an acid to the body, bicarb will buffer
AG=Na- (Cl + HCO3) LA (shock, ATP dec)-->hypoxia, cirrhosis alcohol, phenformin ketoacidosis--DKA (AcAc, BOHB, alcohol BOHB, starvation) renal failure- retention of organic acids salicylate poisoning--pain syndrome esp in RA, prim resp alkalsosi, uncoupler ethylene glycol--oxalic acid, antifreeze RF methyl alcohol--windshield wiper fluid, formic acid, blind met acidosis |
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AG equation
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AG=Na (cl + HCO3)
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pH equation for compensation
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pH=HCO3/PaCO2
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drainage of the ovary venular
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pampiniform plexus-->ovarian vein-->renal vein-->IVC
drainage form the gonadal veins enters the L renal vein-->IVC |
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uncompensated/compensated for alkalosis/acidosis means?
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compensation does not go outsdie reference interval; partial--comp outside reference interval but pH close to normal
full compensation not exist |
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what deals w/ Co2 what deals with bicarb?
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lungs-couple hours
kidney--bicarb |
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ST elevation is seen in what situations?
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MI, thoracic aortic disseciton, pericarditis
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bundle branch block seen in what situaitons?
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in the heart mm and conducting system damage
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normal AG acidosis
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<30 Na-Cl + bicarb
loss of bicarb, not reclaiming in PT, or not making it loss--diarrhea, bile, pancreatic secrtions proximal RTA type 2--can't reclaim distal RTA type 1--can't regenerate, ATP pump in CT way to get rid of excess H+ ions gain bicarb (NaH2Po4 titratable acid or ammonium cloride); light chain in MM damage this pump, amphotericin B; de novo bicarb T2 proximal RTA--reclaiming bicarbonate; Na/H+ pump; not de novo bicarb peed it out combined with teh H+ resorb it break it down then resorp bicarb; lead poisoning |
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vomiting is metabolic
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alkalosis
bicarb >28, bicarb stays in the blood stream |
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barbituates resp?
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acidosis
suppess CNS |
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pulmonary embolus resp?
|
alkalosis to compensate for lack of blood flow
|
|
|
myxedema
|
GAGs--hyaluronic acid
graves-pretibial hashimotos--periorbital |
|
|
what makes proteins?
|
liver; cirrhosis
|
|
|
inc hydrostatic pressure froom what?
|
RHF-pitting; LHF-pulm edema
|
|
|
cirrhosis
|
portal vein HTN builds up hydrostatic pressure...ascites
dec oncotic pressure cant make albumin esophageal varices, splenic vein, sup mesenteric vein--splenomegaly, hemorroids |
|
|
venous thrombosis
|
endothelial injury, venous DVT in leg below knee w/ stasis-->femoral vein, hypercoag can be upper and lower
damaged endothelial cell-->act F8-->fibrinogen -->fibrin; RBCs, WBCs, plts trapped by fibrin after local activation of coagulation system propagates toward heart prevent w/ warfarin and heparin |
|
|
arterial thrombus what prevents?
|
aspirin prevents aggregation-->can cause epistaxis
also ticlopidine and clopidogrel use statins to decrease LDL |
|
|
arterial thrombus from?
|
plts stick after endothelial injury stick w/ fibrin commonly atherosclerosis
disrupted plaque |
|
|
what prevents venous thrombus
|
warfarin and heparin b/c it has plts and RBCs, WBCs
|
|
|
kawasaki disease
|
fever for 5 days, ansyeusms
mucocutaneous LN MCC of heart disease in children desquamative rash of fingers, b/l conjuntivitis, rash oral lesions, fissures pharynegeal erythema, strawberry tongue necrosis, inflammation angina, damage to coronary vessels; sudden death from aneurysm |
|
|
abdominal aortic aneuysms caused by?
|
atheroscerlosis in older men >55
back, abdominal or flank pain |
|
|
claudication caused by?
|
atherosclerosis; dec arterial pulse at ankles; inc peripheral vascular resistance; high lipids
|
|
|
saddle embolus
|
pulmonary embolus; femoral vein site of origin from DVT
|
|
|
arterial embolization
|
originate from Left heart; HEMORRHAGIC infarction (embolus to MCA),
|
|
|
amniotic fluid embolsim
|
ARDS -->DIC; lanugo hair in maternal pulmonary arteries; fetal cells in mom
|
|
|
decompression sickness caused by?
|
nitrogen gas tubbles
hemiperesis dyspnea and pleuritic chest pain-->pulm embolus spont pneumothorax rising to surface fast |
|
|
carotid occlusion
|
tricks the body into thinking low BP-->inc sympathetic tone, dec para due to baroreceptor
give M2 receptor antagonist to inc HR |
|
|
hypovolemic shock
|
blood loss MC; cold calmmy
inc PVR act RAA system (potent VC); dec LVEDP volume loss dec CO; dec MVO2 catacholamine, AT2, ADH effect all VC vessels-->cold clammy skin |
|
|
cardiogenic shock
|
cold clammy skin; dec CO; inc PVR and LVEDP
dec MVO MI forward failure blood remaining behind |
|
|
septic shock
|
gram - sepsis
endotoxins damage endothelial cells release NO (VD, relaxes sm), PGI2 (prostacyclin) act complement system-->release anaphylatoxins C3a c5a stim mast cells to release histamine warm skin, dec PVR, dec LVEDP (amount of blood in arteriole system while heart filling in diastole controlled by arterioles), inc CO; inc MVO2 |
|
|
systolic pressure
|
SV x HR
|
|
|
LVEDP
|
amount of blood in arteriole system while heart filling in diastole controlled by arterioles
|
|
|
exercise causes?
|
VD to dec vascular resistance; inc bf to mm
inc bp in downsterams arterioles inc lymph flow to mm |
|
|
nonsense mutation example
|
B thalassemia major
|
|
|
missense mutation (2)
|
sickle cell disease (valine replaced glutamic acid) and marfan syndrome
|
|
|
down syndrome genetics
|
simean crease, alzeimer's disease 40; risk inc maternal age, CV cusion defect, duodenal atresia, hirschsprung, ALL
nondisjunction (47 unequal separation) robertsonium translocation (46 chrom)-->from mother has 14:21 attached but only count it as 1 so still have 3 21's |
|
|
robertsonium translocation
|
in down's 46 chormosomes
21:14 |
|
|
nondisjunction
|
translocation in meiosis 1; uneual separation
in meiosis 2 fertilized egg would have 47 chrom w/ 3 chorm 21's =down's in meiosis 1 more change 2:4 chance to inc risk of down's |
|
|
tumors of epithelial tissue
|
ectodermal/endodermal derived
carcinoma--usually lymphatic FIRST-->hematogenous benign: adenoma cytokeratin is a marker |
|
|
tumors of CT
|
mesodermal origin
mm, bone, fibrous tissue, fat SARCOMA malig; benign lipoma (MC in males) leiomyoma (uterus MC) love to mets hematogenously first! vimentin is a marker |
|
|
adenomatous poly can become
|
tumor
|
|
|
osteogenic sarcoma
|
malignant tumor of bone MC sarcoma
sunburst |
|
|
squamous cell carcinoma
|
hypercalcemia, PTH
|
|
|
lymphomas marker
|
CD45
malignancy of LN goes to peyers patches and stomach |
|
|
leukemia
|
malignancy of stem cells in bm
|
|
|
malignants cells what happens to them
|
receptors for laminin (bm), fibronectin (ECM), longer clel cycle, atypical spindles, upreg telomerase
cadherins interceullar adhesions--lose attachment-->seeding |
|
|
mets to liver by?
|
colon and liver (smoker)
|
|
|
IL-1 aka
|
osteoclast activating factor
osteolytic, fracture risk |
|
|
PTH related peptide
|
osteoclastic activated BUT NO LYTIC LESIONS IN BONE
|
|
|
cancers in children
|
#1 ALL>leukemia>CNS>neuroblastoma, wilm's >NHL/HL
|
|
|
incidence
|
new cases over time
|
|
|
prevalence
|
at one time
|
|
|
incidence/mortality F cancer
|
breast, lung colon incidence
lung>breast>colon mortality |
|
|
incidence/mortality M cancer
|
incidence in prostate, lung colon
mortality lung>prostate>colon |
|
|
gynecological cancer incidence/mortatlity
|
incidence: endometrial>ovarian>cervical
mortatlity--ovarian>endometrial>cervical US |
|
|
retinoblastoma
|
sporadic (both must have 2 separate hits after birth)
genetic-AD type assoc osteogenic sarcoma (usually in the knee) 2 hit theroy chrom 13--1 already inact in utero white eye reflex |
|
|
familial adenomatous polyposis
|
100% penetrance; AD
always get disease total colectomy POLYPS NOT PRESENT AT BIRTH |
|
|
L gonadal vein vs right
|
left goes into renal; right drains directly into IVC
|
|
|
G6PD and what causes it's hemolysis
|
AR
NItro/sulfur drugs, dapsone, primaquine, quinine produces NADPH to keep glutithiane reduced and detox FRs |
|
|
acute intermittent porphyria
|
AD women,
precipitated by drugs sulfa, phenobarbitol abdominal pain, fever, peripheral neuropathy, paralysis, diaphoresis, restless, weak, onset at puberty leukocytosis, inc porphobilinogen, delta-ALA inc **porphobilinogen deaminase def versus--prophyria cutanea tarda--uroporpphyrinogen decarboxylase def-->phototox, skin inflamma, blistering, cirrhosis assoc, AD, late onset |
|
|
portal vein made up of?
|
superior mesenteric vein and splenic vein
gastric veins from stomach-->esophagus superior rectal veins w/ middle/inf rectal (internal hemorroids) portal vein-->liver sinusoids-->hepatic vein-->IVC |
|
|
rickessia ricksiae 2 diseases
|
RMSF and francisella tularensis
|
|
|
NO
|
vasodilates via guanylate cyclase -->cGMP-->sm relax
|
|
|
kartagener's syndrome
|
immotile cilia due to a dynein arm defect. male and female infertility (sperm immotile0, bornchiectasis, and recurrent sinusitis
bact and particles not pushed out asso cw/ situs inversus MT in 9+2 arrangement, ATPase |
|
|
ehlers-danlos syndrome
|
collagen synthesis
hyperextensible skin, bleed easy bruise, hypermobile joints AD or AR joint dislocation , berry aneurysms, organ rupture collage type 3 |
|
|
osteogenesis imperfecta
|
genetic bone disorder brittle obne diseae
MC is AD w/ abnormal T1 collagen fractures, blue sclerae, hearing loss, dental imperfections (lack dentin) confused w/ child abuse T1 fatal in utero |
|
|
alport's syndrome
|
T4 collagen defect MC is XR
hereditary nephritis and deafness; ocular disturbances impt in basement membrane of kidney, ears and eyes |
|
|
marfan's
|
defect in fibrillin of elastin (proline and glycine nonglycosylated); inhibited by A1-antitrypsin
stretpy material lungs, large arteries, ligaments, vocal cords |
|
|
emphysema
|
AAT def excesselastase activity act on elastin
|
|
|
anticipation
|
disease worsens or age of onset of disease is earlier in succeeding generations
ie Huntington's |
|
|
mosaicism
|
body has diff genetic makeup in cells
--germ-line mosaic disease NOT carrier by parents lyonization--random X inactivation in females |
|
|
3 things that can cause marfanoid habitus?
|
marfan's syndrome, MEN2B, homocytinuria
locus heterogenity--mutations at diff loci can produce the same phenotype |
|
|
imprinting
|
1 locus, 1 allele is active the othe r(inactivated by methylation); deletion of active allele = disease
both by inact or deletion of genes on chrom 15 can also be by uniparental disomy (2 copies of chrom from 1 parent) maternal vs parenteral prader-willi syndrome, angelman's syndrome |
|
|
prader-willi syndrome
|
deletion of normal activ parenteral allele
mental retardation, hyperphagia, obesity (overeat), hypogonadism, hypotonia, short |
|
|
angelman's syndrome
|
deletion of maternal allele in imprinting chrom 15
mental retardation, widebased gait (marionette), inappropriate laughter (happy puppet), seizures ataxia |
|
|
Autosomal recessive
|
1:4 offspring are affected
enzyme deficiencies often; 1 generation more severe tha domiant often in childhood |
|
|
x-linked recessive
|
sons 1:2 chance w/ heterogenous mother; no male to male transmission
more severe in males |
|
|
x linked dominant
|
through both aprents either male or female affected
mother may be affected; all female offspring of affected father are diseased **hypophophatemic rickets |
|
|
hypophosphatemic rickets
|
vit D resistant rickets; inc phosphate wasting in proximal tubule-->ricket's like presentation
|
|
|
mitochorndiral inheritence
|
only through mother; all offspring of affected females show signs of disease
variable expression due to heteropalsmy mitochorndrial myopathies, Leber's hereditary optic neuropathy |
|
|
Leber's hereditary disease
|
mitochondrial inhertiance; degen of retinal ganglion cells and axons leads to acute loss of central vision
optic neuropathy |
|
|
incidence
|
number of new events in a specified period of time/# of people exposed to risk
|
|
|
prevelance
|
all cases at 1 period/total population at risk
|
|
|
hemolytic anemai 2 types
|
G6PD-heinz bodies of Hb as cell lyses
PK pyruvate kinase (AR)--no heinz bodies--inc 2, 3 BPG galactokinase def Gal-1-p-uridyl tranferase def fructosuria--fructokinase def and alolase B def |
|
|
2 bugs affecting EF-2
|
pseudomonas and diptheriae
|
|
|
chemotaxis completments
|
C5a, LTB4 and IL8
|
|
|
A1 receptors
|
smooth muscle contraction Gq
|
|
|
A2 receptors
|
inhibits NT release Gi
|
|
|
B1 receptor
|
inc HR and contractility Gs
|
|
|
B2 receptor
|
sm relaxation Gs
|
|
|
M1
|
affects CNS, PNS, gastric parietal
|
|
|
M2
|
dec HR and contractility
|
|
|
M3
|
stim glandular secretions
|
|
|
cornybacterium diptheriae test
|
ELEK test--contains prophage DNA
gram + rods COBEDS-cholera toxin, o angitgen of salmonella, botulism exotoxin, erythrogenic toxins of streppyogens, diptheria toxin, shiga toxin) |
|
|
china has?
|
nasopharyngeal carcinoma--EBV
|
|
|
japan has?
|
stomach adenocarcinoma (smoked foods)
|
|
|
SE asia has?
|
HCC (HBV + aflatoxins in peanuts)
HBV is a tumor vaccine |
|
|
africa?
|
burkitt's EBV-jaw; US-paraortic, kaposi's sarchoma HHV8
|
|
|
xeroderma pigmentosum
|
AR, defect in DNA repair enzymes cannot excise pyrimidine dimers; BCC, SCC
|
|
|
fiber in women
|
sucks up estrogen from blood stream and get rick of it
endometrial cancers, breast cancers decrease |
|
|
2 tumor vaccines
|
HPV, HBV
|
|
|
H pylori treatment prevents
|
lymphoma and stomach adenocarcinoma
|
|
|
#1 mutation producing cancer
|
point mutation TP53 and Rb supressor and Ras
|
|
|
9:22
|
CML
philadelphia fusion gene; bcr:abl |
|
|
14:18
|
follicular lymphoma
|
|
|
8:14
|
burkitt's
|
|
|
15:17
|
APL leukemia
|
|
|
ERBB2
|
amplificaiton; breastcancer bad prosgnostic sign for breast carcinoma
|
|
|
BCl2 carcinogen?
|
overexpression---never turned off, working harder; inhib release of cyt C no apop
|
|
|
proto-oncogenes
|
potential for becomes cancer
ERBB2, RAS, ABL, MYC; receptors for growth factors |
|
|
Ras POC
|
GTP signal transduction; point putation
messenger system leukemia, lung, colon, pancreas |
|
|
Abl POC
|
non receptor tyrosine kinase; 9:22
messenger system CML |
|
|
MYC
|
nuclear transcription
8:14, burkitt's "monk's" vs N-myc amplification neuroblastoma |
|
|
BRCA
|
regulates DNA repair
breast ovary prostate |
|
|
APC
|
prevents nuclear transcription
famial polyposis |
|
|
RB
|
prevents G1-->S
lung, colon, breast |
|
|
mismatch sysdrome
|
lynch syndrome
--repair genes bad |
|
|
TP53
|
inhibits G1-->S, lung cancer, colon breast
repeairs DNA, act BAX Li-Fraumeni |
|
|
clear cell carcinoma of vagina from?
|
DES
|
|
|
EBV produces
|
burkitt's, CNS lymphoma (AIDS), HL mixed cellularity; nasopharyngeal carcinoma
|
|
|
clonorchis sinesis
|
cholangiocarcioma
|
|
|
2 parasites producing cancer
|
schistosoma hematobium clonorchis sinesis
|
|
|
pyrimidine dimer (thymine ) repaired?
|
endonuclease 1st DNA repair enzyme-->exonuclease excises out pyrumidine dimers-->polymerase 5 to 3 synthesis new strand w/ base matching-->ligase joins strands
|
|
|
eaton-lambert syndrome
|
antibody aginst calcium channel kinda like myasthenia gravis
related to small cell carcinoma of lung |
|
|
markers for pancreatic carcinoma
|
superficial migratory thromboplebitis-trousseus's sign, NBTE (non bact thrombotic endocarditis mitral valve)
|
|
|
2 markers for stomach cancer
|
seborrheic keratosis (leser trelat), acanthosis nigricans
2 pigmented lesions |
|
|
small cell carcinoma can produce****
|
ACTH-->ectopic cushing's
ADH hyponatremia <120 serum Na |
|
|
choriocarcionma can produce?
|
HCG, gynecomastia
|
|
|
RCC carcnioma can produce?
|
EPO polycythemia
PTH related eptide hypercalcemia |
|
|
HCC can produce?
|
EPO polycythemia
ILF hypoglycemia |
|
|
medullary carcinoma of thyroid can produce
|
calcitonin hypocalcemia****
ACTH ectopic Cusching's |
|
|
squamous cell carcionoma can produce?
|
PTH related peptide hypercalcemia
|
|
|
Ca125
|
ovarian
|
|
|
AFP in what cancer
|
albumin in a fetus-->HCC, yolk sac (testicle, ovary)
|
|
|
BJ protein what cancer
|
MM, waldenstrom's-lymphoma no lytic lesions, IgM monoclonal spike
|
|
|
CEA what cancer
|
colorectal cancer, pancreas
|
|
|
reticulocyte count equation
|
Hct/45 x retic count /polychromasia
RNA filaments; young cells |
|
|
extramedullary hematopoiesis see in
|
sickle cell and B thal
myelofibrosis; hair on end, frontal bossing chipmunk cheeks |
|
|
mature RBCs describe?
|
no mitochondria or HLA just match blood groups, anaerobic glycolysis energy source
metHb reductase, pentose phosphate shunt (glutithione), synthesis of 2,3 BPG (OBC) form 1, 3BPG |
|
|
iron def child, women/man <50; >50
|
inadequate intake and Meckel's divertic; menorrhagia, PUD; colon cancer
|
|
|
hepcidin
|
acute phase reactant---blocks iron from getting out of macs
inc ferritin in anemia of chronic disease malignancy and alcoholics |
|
|
3 diseases w/ iron overload
|
sideroblastic anemias, hemochromatosis, hemosiderosis
|
|
|
aplastic anemia
|
pancytopenia; NOT LYMPHOCYTES B/T CELL defect/inhib myeloid stem cells; dec RBCs, leukocytes, plts
drugs alkylating agens, chloramphenical, parvovirus HCV (infection), benzene, IR SEE FAT AND LYMPHOCYTES in marrow |
|
|
blood doping
|
save own blood or give EPO
|
|
|
extravascularly hemolysis
|
IgG and C3b warm;
jaundice, UCB, macs; shape can't enter vessels in cord of liver |
|
|
intravascular hemolysis
|
mechanical injury NO MACS, HEMOBLOBINURIA
IgM, dec haptoglobin damage (forms a complex w/ Hb that is lost so macs can phagocytose both) no jaundice; + dipstick for blood |
|
|
spherocytosis
|
AD, mutation in akyrin in cell membrane and Na/Kase test not function so osmotically fragile
inc MCHC spleen removes -->SM; extravascular ca-bilrubinate stones-BLACK splenectomy but first pneumovax to prevent strep pneumo, HI, salmonella |
|
|
PNH
|
complement deposits at night on myeloid stem cells; DAF degrades complement usually CD59
pancytopenia, hemogblinuria; postive sugar water test (makes complement already on cells) and acidified serum test intravascular vessel thrombosis, AML |
|
|
sickle cell
|
AR, intrinsic extracellular
missense mutation sticky cells block small vessels >60% HbS-->spont sickle |
|
|
how to increase HbF?
|
hydroxyurea in sickle cell
|
|
|
2 things cause target cells
|
alcoholic, sickle cell....anemia
|
|
|
howell jolly bodies
|
sickle cell....dysfunctional spleen
|
|
|
heinz bodies
|
in G6PD disease-->bite cells
during hemolysis enzyme assay will show dec level in affect RBCs post-hemolysis |
|
|
enzyme assay when in G6PD
|
post hemolysis; bite cells NOT heinz bodies
|
|
|
pyruvate kinase def
|
dec ATP in
phosphoenolpyruvate-->pyruvate gain2 atp but 2,3 BPG inc b/c prox to this echinocytes b/c damaging RBC mmembrane from dysfunctional Na/K atpase pump in membrane AR, intrinsic extravascular |
|
|
direct coombs
|
Direct coombs—rabbit IgG or C3b given to RBCs w/ Ab agglutinate; look for it ON RBCs
|
|
|
indirect coombs
|
Indirect coombs—looking for antibody unidentified in serum, pregnant women,
|
|
|
example of cold antibodies disease
|
M pneumoniae anti I
|
|
|
penicillin anemia
|
antibody directed against PCN; T2HS
extrinsic, extravascular |
|
|
quinidine anemia
|
immunocomplex w/ IgM
T3HS extrinsic, intravascular |
|
|
methyldopa anemia
|
T2HS, extrinsic, extravascular
against Rh; antibodies against damaged Rh antigens NOT the drug ---pregnancy and HTN BUT 20% have + direct coombs |
|
|
MIHA
|
extrinsic, intravscular hemoglbinuria
schistocytes and aortic stenosis--can get iron def must remove valve |
|
|
p vivax
|
tertian 48 hrs
MC malariae extrinsic, intravascular; rupture of rBCs correspons w/ fever patterns |
|
|
falciparum malarie
|
quotian daily spikes no pattern
chronic malarie extrinsic, intravascular; rupture of rBCs correspons w/ fever patterns ring forms only |
|
|
p. malarie
|
quartan 72 hours
extrinsic, intravascular; rupture of rBCs correspons w/ fever patterns |
|
|
schistocytes causes
|
TTP, MIHA, HUS, DIC
|
