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317 Cards in this Set
- Front
- Back
What does null hypothesis mean
|
no difference exists
|
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How do you define type I error?
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incorrectly rejects the null hypothesis
|
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what is type II error?
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incorrectly accepts the null hypothesis
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What is type III error?
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conclusions are not supported by data
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How is a prospective cohort study arranged?
|
non-random assignment to treatment group
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What is a meta-analysis?
|
review and combining of statistics from data of different studies
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What is an ANOVA t-test for?
|
more than 2 samples of quantitative data
|
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What are non-parametric statistics for?
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Qualitative data analysis
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What are nominal qualitative variables?
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named variables, such as color
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What are ordinal qualitative variables?
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Arranged on a scale, such as pain from 1-10
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What is prevalence?
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Number of people having a disease in a population studied; prevelance is higher in long-lasting non-fatal diseases
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What is incidence?
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The number of newly diagnosed cases of a disease in a population over time, usually yearly.
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What is sensitivity?
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the ability to detect disease
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What is the equation for sensitivity? (+result and true +)
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positive test results / true positives
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What is specificity?
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Ability to state that no disease is present
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Equation for specificity
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negative test results / (true negatives + false positives)
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What cell is the source of fever in atalectasis?
|
Alveolar macrophages
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What are the cellular characteristics of mitochondria?
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2 membranes with an inner matrix
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What cycle takes place in the inner matrix of mitochondria?
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TCA cycle
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How do the rough endoplasmic reticulum and outer membrane of nucleus relate?
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they are continuous
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Where are ribosomes made?
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Nucleolus, which has no membrane
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What proteins are made in the rough endoplasmic reticulum?
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proteins for export
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What proteins are made in the smooth endoplasmic reticulum?
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cytoplasmic proteins
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What are the contents and proportions of the plasma membrane?
|
60%protein, 40% lipid.
|
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higher cholesterol in membrane equals ______ of proteins
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higher mobility
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Symptoms/ exam findings of malignant hyperthermia
|
fever, tachycardia, rigidity, acidosis
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cause of malignant hyperthermia
|
calcium release from sarcoplasmic reticulum
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First sign of malignant hyperthermia?
|
increased end-tidal CO2
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What is the treatment for malignant hyperthermia?
|
Stop operation and anesthetics, give dantrolene and supportive care
|
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T/F: Malignant hyperthermia usually occurs at a patient's first exposure to anesthesia.
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False, usually not first exposure
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What are the first and last muscles to recover from paralytics?
|
First: Diaphragm. Last: neck and face.
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What type of tissues don't have lymphatics?
|
Muscle, bone, tendon, brain
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How are the cells of lymphatics joined?
|
Loosely in a cell to cell junction. No basement membrane.
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What is the rate limiting step in cholesterol formation?
|
HMG co-A reductase, steroid precursor found in the liver
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What part of the target cell do steroid hormones go to?
|
They are bound in the cytoplasm before going to the nucleus.
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What are the initial and final products of the Krebs cycle?
|
one glucose makes 38 ATP
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What are the initial and final products of anaerobic glycolysis?
|
one glucose makes 2 ATP and a lactate
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What drugs increase Cytochrome p450 activity?
|
anticonvulsants, coumadin, theophylline
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What drugs decrease Cytochrome p450 activity?
|
cimetidine, INH, MAOIs, disulfiram
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What makes renin?
|
Macula Densa
|
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What does the macula densa sense?
|
low Sodium and chloride levels
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Action of renin
|
converts angiotensinogen to Angiotensin I
|
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What converts Angiotensin I to II? Where?
|
Angiotensin converting enzyme, in the lung
|
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What is the action of angiotensin II?
|
vasoconstrictor, increases aldosterone
|
|
Electrolyte changes with aldosterone
|
retaining sodium; losing potassium and hydrogen in the urine
|
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What changes occur with renal osteodystrophy?
|
The kidney loses calcium and retains phosphorus, causing decreased Vit D hydroxylation
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What is renal osteodystrophy
|
secondary hyperparathyroidism
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Hepatic branch comes off which part of the vagus?
|
left (anterior)
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What branch does the right vagus give off?
|
Celiac branch and criminal nerve of Degrassi
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Why is it the "criminal" nerve of Degrassi?
|
Can lead to high post-vagotomy acid levels if undivided
|
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Which pathway is measured by ptt?
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intrinsic pathway
|
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What triggers the intrinsic pathway?
|
exposed collagen
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Which pathway triggers factor X?
|
both intrinsic and extrinsic
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How does factor X lead to clot formation?
|
X activates thrombin to produce fibrin
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Which pathway is measured by PT?
|
extrinsic pathway
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What triggers the extrinsic pathway?
|
tissue factor
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____ crosslinks ____ to form "plug"
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Factor XIII; fibrin
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What is the best single test to evaluate synthetic function of the liver
|
PT
|
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Banked blood is high or low in 2,3 DPG? increases or decreases O2 affinity?
|
low; decreases O2 affinity (left shift)
|
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Which blood product contains fibrinogen and VWF-III?
|
Cryoprecipitate
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In what bleeding disorders is cryoprecipitate used in?
|
von willebrand's disease, hemophilia A, DIC if fibrinogen is low
|
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Which factors are inhibited by coumadin?
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Vit K: 2, 7, 9, 10, protein C and S
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What is the action of protein C? and S?
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C degrades active Factor V and VIII, S helps.
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Factors V and VIII are at ____ levels in stored blood
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low- these factors are labile
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What is the only factor not made by the liver?
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Factor VIII
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What are the coagulation test findings in Von Willebrands?
|
long PTT, long bleeding time, positive ristocetin test
|
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What is the difference between Type I and III Von Willebrand disease and Type II?
|
I and III: low levels of von willebrand's factor, whereas II has qualitatively poor vwf.
|
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What product is useful in von Willebrands Type I and III and why?
|
DDAVP- causes von willebrand factor release
|
|
DDAVP is useful in what bleeding dyscrasias?
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TYpe I and III VW disease, uremic platelet disfunction, pts on aspirin
|
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What bleeding dyscrasias are autosomal dominant?
|
von Willebrand's, Rosenthal's XI deficiency
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What is the one inherited coagulopathy with a long bleeding time?
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Von Willebrand's
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What is Glanzmann's thrombasthenia?
|
IIb/IIIa receptor deficiency in platelets, with decreasing platelet aggregation
|
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What is Bernard Soulier disease?
|
Ib receptor deficiency in platelets, decreased adherence to exposed collagen
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PT/PTT results in Factor VII deficiency
|
long PT, normal PTT
|
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What is hemophilia A?
|
sex-linked recessive factor VIII deficiency
|
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To what % should Factor VIII be replaced pre-operatively in hemophilia A?
|
100%
|
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PT/PTT results in hemophilia A
|
long PTT, normal PT
|
|
Treatment for a hemophiliac joint
|
Do NOT aspirate. ice, range of morion therapy, give factor VIII
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What is hemophilia B?
|
sex-linked factor IX deficiency (Christmas disease)
|
|
To what % should Factor IX be replaced pre-operatively in hemophilia B?
|
50%
|
|
What is lupus anticoagulant?
|
antiphospholipid antibodies, generally pre-coagulant and not associated with Lupus
|
|
How can you diagnose lupus anticoagulant?
|
long Russel Viper venom time, long PTT which does not correct by adding normal plasma
|
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Why is heparin needed in cardiopulmonary bypass?
|
Factor XII is activated by bypass
|
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What is Factor V Leyden?
|
activated protein C resistance (common cause of DVT)
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Plasmin degrades ____ and is inhibited by _____
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fibrinogen; alpha-2-plasmin inhibitor
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What is the mechanism of heparin?
|
Binds and activates antithrombin III and inactivates Factors 9-12
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How does heparin change coag levels?
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elevates PTT
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How do you reverse heparin?
|
protamine
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Treatment for thrombolytic overdose; how does it work?
|
epsilon-aminocaproicacid (E-ACA) inhibits fibrinolysis
|
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Best test to moniter thrombolysis?
|
thrombin time
|
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Lab values in DIC
|
low platelets, prolonged PT/PTT, low fibrinogen, high fibrin split products
|
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What is HIT?
|
"white clot syndrome": anti-platelet antibody causing platelet aggregation and thus thrombocytopenia
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When after heparin does HIT usually occur?
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about 5 days
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True or false: HIT doesn't occur with low molecular weight heparin
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False, it occurs but less frequently
|
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Action and origin of prostacyclin?
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decreases platelet aggregation, vasodilation, bronchial relaxation. from endothelium
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Action and origin of thromboxane
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increases platelet aggregation, causes vasoconstriction; from platelets
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Best pre-op test for patient on NSAIDs or aspirin?
|
bleeding time
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Where is pepsinogen produced?
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Chief cells
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Action of pepsinogen?
|
initiates proteolysis
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Cell of origin for intrinsic factor
|
binds B12, absorbed in the terminal ileum
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Main stimuli for H+ production?
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Acetylcholine, Gastrin, Histamine
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How do Ach and gastrin work to produce acid?
|
activate PIP system, releasing calcium to activate protein kinase C to increase HCl production
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What cells does histamine work on and via what?
|
acts on parietal cells via cAMP to increase HCl
|
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What cells produce gastrin?
|
Antral G cells
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What inhibits gastrin production?
|
acidification of duodenum
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What stimulates gastrin production?
|
Acetylcholine, amino acids in duodenum
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Action of omeprazole?
|
blocks hydrogen/potassium ATPase in parietal cell
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Effects of somatostatin
|
decreases gastrin, insulin, secretin, acetylcholine, pancreatic output, biliary output.
|
|
What stimulates somatostatin?
|
acid in duodenum
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Effects of proximal vagotomy on stomach emptying liquids?
|
increased liquid emptying by abolishing receptive relaxation
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Effects of proximal vagotomy on stomach emptying solids?
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no change
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Effects of truncal vagotomy on stomach emptying solids?
|
increased emptying when pyloroplasty done
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Most common post-vagotomy symptom
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Diarrhea- 35%
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How common is post-vagotomy dumping syndrome?
|
10%
|
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Physiology of early dumping syndrome post-vagotomy
|
hyperosmotic load causing fluid shift
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Physiology of late dumping syndrome post-vagotomy
|
increased insulin, low glucose
|
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Usual treatment for dumping syndrom?
|
except 1%, responds to dietary measures
|
|
What activates trypsinogen into trypsin
|
enterokinase
|
|
Where is CCK secreted from
|
intestinal mucosa
|
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Actions of CCK (3)
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gallbladder contraction, sphincter of Oddi relaxation, increased pancreatic enzyme secretion
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What is the primary stimulus of pancreatic bicarb secretion?
|
Secretin
|
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High flow rate in the pancreas causes high or low bicarb, high or low chloride?
|
high Bicarb, low chloride
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how does flow rate affect the bicarb and chloride concentrations in the pancreas?
|
Slow flow allows the HCO3/Cl exhange to occur; slow flow is low bicarb, high chloride
|
|
Action of enteroglucagon?
|
increased small bowel mucosal hypertrophy, including adaptation after bowel resection
|
|
What secretes Peptide YY?
|
terminal ileum (in setting of proteins and carbs)
|
|
What is the action of Peptide YY?
|
"ileal brake"; acid secretion is inhibited
|
|
Contents of bile
|
80% bile salts, 15% lecithen, 5% cholesterol
|
|
When do stones form in bile?
|
if too much cholesterol or too little salts or lecithin
|
|
How is bile concentrated?
|
Active reabsorption of Na, Cl, followed by water in the gallbladder
|
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How large is the bile pool and how much is lost daily? how often is it recirculated?
|
5 grams, 0.5 grams lost daily (10%). recirculates q4 hours
|
|
What are the primary bile acids?
|
Cholic acid, chenodeoxycholic acid.
|
|
What are secondary bile acids? how do they form?
|
deoxycholic acid, lithocholic acid- formed by intestinal bacteria
|
|
What is the MMC?
|
interdigestive motility
|
|
How long are MMC cycles?
|
90 minutes
|
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What organs are involved in MMC?
|
stomach through terminal ileum consecutively
|
|
Describe MMC phase I
|
quiescence
|
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MMC Phase II
|
gallbladder contraction
|
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MMC phase III
|
peristalsis
|
|
MMC phase IV
|
subsiding electrical activity
|
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What is the stimulatory hormone for MMC?
|
motilin
|
|
how does erythromycin's prokinetic activity work?
|
stimulates motilin receptor
|
|
Which is more permeable to water, ileum or jejunum?
|
Jejunum- paracellular absorption of sodium and water
|
|
What stimulates B cells to become Ab-secreting plasma cells?
|
IL 4
|
|
What are opsonins?
|
Ig's that can fix complement: IgG (2) or IgM (1)
|
|
What operation decreases IgM levels?
|
splenectomy
|
|
What immunoglobulin is made first?
|
IgM
|
|
What immunoglobulin is in secretions?
|
IgA
|
|
What is the primary serum Ig?
|
IgG
|
|
Which Ig crosses the placenta?
|
IgG
|
|
What Ig is involved in parasitic reactions and allergic reactions?
|
IgE
|
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What Ig is involved in Type I hypersensitivity?
|
IgE
|
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Which region of the antibody is responsible for antigen recognition?
|
variable region
|
|
Which complement factors are anaphylatoxins?
|
C3a, C5a
|
|
Which parts of complement make the MAC?
|
C5-9
|
|
What activates the classic complement cascade?
|
antibodies
|
|
What activates the alternate path?
|
bacteria
|
|
Where do the classic and alternate paths meet?
|
C3
|
|
What does MHC class I activate?
|
CD8 cells
|
|
Where is MHC I found?
|
all nucleated cells
|
|
What does MHC class II activate?
|
CD4 cells
|
|
Where are MHC II found?
|
B cells, dendrites, monocytes
|
|
What is responsible for immunosurveillance against cancer?
|
Natural Killer cells- they recognize cells without self-MHC
|
|
What is the action of IL2 on natural killer cells?
|
converts them to Lymphokine activated killers
|
|
Is a Natural Killer Cell a T cell or B cell?
|
neither, no antigen presentation needed, they recognize any cell without a Self-MHC
|
|
Best test to evaluate cell-mediated immunity?
|
intradermal skin test
|
|
Source of histamine in the blood?
|
basophils
|
|
Source of histamine in the tissue?
|
mast cells
|
|
Endotoxin is from what type of bacteria?
|
gram negatives
|
|
What makes up endotoxin?
|
lipopolysaccharide A
|
|
Causes for SVo2>77%?
|
cyanide or sepsis
|
|
Effects of sepsis on glucose?
|
Hyperglycemia comes 24hrs before overt sepsis
|
|
how does sepsis effect oxygenation?
|
decreases oxygen extraction, so increased SVO2, decreased delta A-V O2
|
|
Possible locations of intrabdominal abscess (4)
|
sub-diaphragmatic, sub-hepatic, interloop, pelvic
|
|
Treatment for C Diff?
|
oral vanco or flagyl
|
|
Infections that present within first few post-op hours
|
Beta-hemolytic strep and Clostridial
|
|
Clear slime with chronic infection is characteristic of what bug?
|
Staph Aureus (coag -)
|
|
How do aminoglycosides work?
|
bactericidal, irreversibly bind to ribosome
|
|
How does resistance to aminoglycosides work?
|
decreased active transport (toward ribosome)
|
|
Clindamycin: bacteriostatic or bactericidal?
|
bacteriostatic
|
|
Erythromycin mechanism of action?
|
reversible binding to ribosome (same as clinda and tetracycline)
|
|
How does vanco work?
|
Binds plasma membrane
|
|
how does vanco resistance work?
|
altered cell wall
|
|
What causes MRSA resistance?
|
altered bacterial binding protein (not beta-lactamase)
|
|
What drugs inhibit beta-lactamase?
|
sulbactam, clavulanate (unasyn and augmentin)
|
|
How does amphotericin work?
|
binds sterols to alter fungal walls
|
|
Side effects of amphotericin
|
renal impairment (80%), fever, anemia
|
|
Action of quinolones?
|
inhibits DNA gyrase
|
|
How does ketamine effect cardiac work? O2 use? blood pressure?
|
increases cardiac work, as well as oxygen usage and blood pressure and secretions
|
|
Effect of ketamine on respiratory drive
|
Respiratory depression
|
|
Side effect of ketamine
|
hallucinations
|
|
Methoxyfluorane is toxic to what organ?
|
kidneys
|
|
Halothane is toxic to what organ?
|
liver
|
|
The only depolarizong agent
|
Succinylcholine
|
|
Risk in burn patients with succinylcholine
|
hyperkalemia
|
|
onset of action with succinylcholine
|
fast on/fast off
|
|
Risks/side effects of succinylcholine
|
aspiration, glaucoma
|
|
What antibiotic prolongs neuromuscular blockade?
|
clindamycin
|
|
Demerol should be avoided in which patients?
|
those on MAOIs
|
|
What is octreotide?
|
long acting somatostatin analog
|
|
Mechanism of metoclopramide
|
Dopamine antagonist, increasing LES tone and gastric motility
|
|
Mechanism of omeprazole
|
H+ ATPase blocker
|
|
Mechanism of digoxin
|
glycoside which inhibits Na-K ATPase pump to increase calcium in the heart, slowing AV conduction, inotropic
|
|
Benefit of digoxin as an intrope
|
doesn't increase O2 consumption
|
|
Side effects of digoxin
|
gut ischemia from decreased splanchnic flow
|
|
Electrolyte imbalance to avoid with digoxin
|
hypokalemia
|
|
Mechanism of amrinone
|
phosphodiesterase inhibitor
|
|
net effect of amrinone
|
Inotropic, increasing CO, decreasing SVR
|
|
Drugs creating medical adrenalectomy
|
metyrapone and aminoglutethimide
|
|
Medical Orchiectomy drug
|
leuprolide
|
|
Drug to give in GI bleed (besides PPI)
|
vasopressin: reduces splanchnic flow and portal flow about 40%
|
|
Drug to give with vasopressin in gi bleed
|
Beta blocker to avoid angina
|
|
Drug that relaxes veins and arteries
|
Sodium Nitroprusside
|
|
Nitroglycerin relaxes arteries or veins?
|
veins
|
|
Aspirin irreversibly binds _____; how long is the effect?
|
cyclooxygenase; 7 days, the life of a platelet
|
|
________ blocks prostaglandin production
|
indomethacin
|
|
how often is indomethacin effective in closing a PDA?
|
70%
|
|
Other effect of indomethacin
|
decreases renal blood flow
|
|
Cytoprotective drug for pt on NSAIDS to reduce PUD?
|
Misoprostil, replaces prostaglandin E2.
|
|
lab values indicating prerenal azotemia
|
FeNa <1, Urine Na < 20, BUN/creatinine ratio >30
|
|
three body fluids with the highest k concentration
|
1) Saliva, 20 mEq
2) Gastric, 10 3) Pancreatic/duodenal, 5 |
|
Which amino acids are metabolized in muscle?
|
branched chain amino acids
|
|
What are the essential amino acids?
|
Leucine, isoleucine, valine
|
|
Where is vitamin D made, what activates it?
|
made in the skin, activate by hydroxylation in liver and kidney
|
|
How do Vitamin D and calcium interact?
|
Vit D increases binding protein to increase intestinal absorption of calcium
|
|
What reverses the effects of steroids on wound healing?
|
Vitamin A, systemic or topical
|
|
Population with highest total body water
|
infants (80%)
|
|
Total body water in men; women.
|
60%; 50%.
|
|
What is the alteration in total body water for obese patients?
|
10% less than normal
|
|
Distribution of water in the plastma, interstitium, cells
|
60% TBW: 40% cellular, 15% interstitium, 5% plasma
|
|
Calories in carbs
|
3.4 kcal per gram
|
|
Protein calories
|
4 kcal per gram
|
|
Fat calories
|
9 kcal per gram
|
|
Basal calorie expenditure and protein need
|
25 kcal/kg/day, 1g protein/kg/day needed
|
|
Resp quotient definition
|
ratio of CO2 produced to O2 consumed
|
|
Resp quotient in fat use
|
0.7
|
|
Resp quotient in carb use
|
1.0
|
|
How much nitrogen in protein?
|
1 g nitrogen in 6.25 g protein
|
|
Preferred fuel of small bowel
|
glutamine
|
|
#1 amino acid in bloodstream
|
glutamine
|
|
glutamine levels ___ in stress due to ____
|
decrease; glutamine goes to kidney to form ammonium to help acidosis
|
|
What protein decreases translocation and aids mucosal health during bowel chemo/RT?
|
glutamine
|
|
What two forms does fat take to be absorbed?
|
micelles absorbed by enterocytes and enter lymphatics. Medium and short chain TG's enter portal system
|
|
Chromium deficiency?
|
hyperglycemia (relative diabetes) neuropathy
|
|
Zinc deficiency
|
perioral rash, hair loss, poor healing, change in taste
|
|
phosphate deficiency
|
resp weakness, encephalopathy due to phophate need for ATP
|
|
Copper deficiency
|
anemia, neutropenia
|
|
Linoleic acid
|
dermatitis, hair loss, vision changes
|
|
Most variable period of cell cycle
|
G1 (growth factors act during it)
|
|
Most sensitive cell cycle phase for RT
|
M
|
|
What makes RT most effective?
|
high O2 levels
|
|
What decreases skin damage from RT
|
higher energy RT
|
|
What is obliterative endarteritis?
|
impaired fibroblasts cause decreased healing after RT
|
|
How do you biopsy an extremity sarcoma?
|
excisional if <4cm, longitudinal incisional biopsy if larger
|
|
Why longitudinal biopsy in sarcoma?
|
less lymphatic disruption, easier to excise scar
|
|
Indications for RT in sarcoma
|
high grade, close margins, tumor >5cm
|
|
Li Fraumeni syndrome
|
p53 mutation causing sarcomas, breast ca, brain tumor, leukemia
|
|
How do sarcomas spread?
|
hematogenously, not via lymphatics
|
|
Mutations in colon cancer (4)
|
loss of APC gene, p53 mutation, DCC (deleted in colon cancer), k-ras activation
|
|
mutations associated with breast ca
|
p53, Bcl-2, cmyc, cmyb, her 2 neu
|
|
Tumors associated with cmyc
|
small cell lung Ca, neuroblastoma, Burkitts lymphoma
|
|
Action of Bcl-2
|
regulates apoptosis
|
|
proto-oncogenes associated with apoptosis
|
BCl-2, p53, cmyc
|
|
oncogene homologous to PDGF
|
SIS
|
|
What does erb b oncogene code for?
|
epidermal derived growth factor receptor
|
|
tumor associated with decreased survival with erb b
|
breast ca
|
|
K ras protooncogene codes for _____
|
GTP protein
|
|
tumors associated with K ras
|
pancreatic (90%), colon (50%), lung ca
|
|
Proto-oncogene diagnostic for medullary thyroid carcinoma
|
Ret proto-oncogene
|
|
Appropriate therapy in a pt with family hx of MEN and + Ret proto-oncogene
|
total thyroidectomy
|
|
Action of tamoxifen
|
binds estrogen receptor, decreases breast ca in high risk pts
|
|
Risks with tamoxifen
|
DVT, endometrial ca
|
|
Chemo drugs causing pulmonary fibrosis
|
bleomycin and busulfan
|
|
Chemo drugs causing neurotoxicity
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vincristine, cisplatin
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What is Levamisole
|
antihelminthic drug, also an immunostimulant (chemo)
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Cells which provide wound contraction
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myofibroblasts
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Cells responsible for healing by secondary intention
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myofibroblasts (contracts from center)
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Principle collagen in scar
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Type I
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Most abundant collagen type
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Type I
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type of collagen deficient in Ehlers Danlos
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Type III
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collagen type in healing wound
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Type III
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Collagen type in basement membrane
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Type IV
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Collagen type in cartilage
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Type XI and II
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What is the structure of collagen?
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glycine x 3
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What enzyme crosslinks collagen
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prolyl hydroxylase
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What cofactors are needed for collagen crosslinking?
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alpha-ketoglutarate, Vit C, O2, iron
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When does collagen production begin?
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Day 3
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When is maximal collagen production?
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Day 21?
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When does collagen crosslinking occur?
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At week 3 (after day 21).
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When does type III collagen become type I?
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week 3
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T/F: tensile strength in healed wound is equal to pre-wound
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False, never equal
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Opening a wound at least 5 days old will heal quicker, slower, or the same the 2nd time?
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Quicker because cells and products are already there
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Reduces harmful effects of steroids on wound healing
|
Vit A
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Name in order the cells appearing in a wound
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platelets, neutrophils, macrophages, fibroblasts
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Cell essential to wound healing
|
macrophages
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growth factor which stimulates fibroblasts
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TGF-beta
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result of too much or too long TGF-beta
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fibrosis (cirrhosis and pulm fibrosis)
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Action of TGF beta
|
stimulates fibroblasts, chemotactic for neutrophils, speeds healing
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Action of PDGF
|
attracts fibroblasts and increases smooth muscle
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Result of PDGF in a wound
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speeds matrix deposition, collagen formation
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Drug used in chemotherapy pts to increase neutrophil and macrophage activity
|
GmCSF
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|
What cells make thromboxane?
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platelets
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Action of thromboxane
|
platelet aggregation, vasoconstriction
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Action of PGI2, prostacyclin
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platelet inhibition, vasodilation, bronchodilation
|
|
Which cytokines respond initially to injury?
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TNF/IL1 (synergistic), Cxc, IL6
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Main source of TNF
|
macrophages/monocyte
|
|
most potent stimulus for TNF production
|
endotoxin (lipopolysaccharide a) from gram negs
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TNF has an anti- or pro- coagulant effect?
|
pro-coagulant
|
|
How does TNF cause cachexia in cancer?
|
lipolysis, glycolysis, anorexia
|
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Result of TNF alpha neutrophil recriutment
|
more cytokines and free radicals, multi-organ system failure in exaggerated response
|
|
Which cells produce IL 1?
|
macrophages, monocytes
|
|
Responsible for fever
|
IL 1
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action of IL 1
|
potentiates TNF, increases IL 6, increases endothelium adherence via selectins, ICAM, VCAM
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|
symptoms of acute phase response
|
fever and catabolism
|
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Substances increased in acute phase response
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CRP, amyloid, fibrinogen, haptoglobin, ceruloplasmin, alpha-1 antitrypsin
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Decreased in acute phase response
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albumin, transferrin, fibronectin
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Cxc chemokine action
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chemotaxis, angiogenesis, wound healing (c for cysteine)
|
|
Active agent in Regranex
|
PDGF
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