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sem 4 > GIT case 5-9 > Flashcards

GIT case 5-9 Flashcards

1
Q

prostate gland fluid secretion contents

A

calcium, citrate ion, phosphate ion, clotting enzyme, profibrinolysin

slightly alkaline

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2
Q

Lower urinary Tract symptoms

A
  • storage symptoms: frequency, urgency, nocturia, urge incontinence
  • voidance symptoms: dysuria, hesitancy, poor stream, terminal dribbling, sensation of incomplete emptying
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3
Q

micturition mechanisms

A
  1. urethral relaxation before detrusor contraction
  2. simultaneous relaxation of pelvic floor muscles
  3. “funnelling” of bladder neck to facilitate flow of urine into proximal urethra
  4. detrusor contration occurs to forcefully expel urine
  • -> underlying activity:
  • increase parasympathetic neuronal activity: removal of central inhibition
  • voiding initiated by pontine medullary centres
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4
Q

different types of incontinence

A
  • urge

- overflow (obstruction): dangerous because can build up and cause back flow

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5
Q

How to measure LUTS

A

International Prostate Symptoms Score IPSS: sefull to see changes over time

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6
Q

examination for prostate (+ LUTS)

A
  • abdominal and genitals (palpable bladder, phimosis)

- DRE

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7
Q

investigations for prostate

A

-UEs, creatinine, eGFR
-PSA
-mid stream urine for infection/haematuria
(-ultrasound urinary tram-kidney and bladder residual volume)

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8
Q

prostate function

A
  • antegrade ejaculation
  • contributes to 25% ejaculate volume
  • sperm nutrition, milieu to thrive, antimicroial (Zn, selenium)
  • PSA enzyme for semen coagulation and liquefaction
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9
Q

pathogenesis of benign prostate hyperplasia

A
  • trauma from voiding bladder causes damage to urethra in transitional zone: produces inflammatory response: local enlargement of cells + lack of apoptosis
  • proliferation of prostate glands, smooth muscle, connective stroma

-age and testosterone are important

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10
Q

alpha adrenergic receptors in prostate

  • location
  • type
A
  • alpha-1 adrenergic receptors

- mainly neck of bladder

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11
Q

alpha 1 blockers

  • names
  • advantages
  • SE
A
  • tamsulosin (flomax)
  • alfuzosin (Xatral)
  • Doxazosin (Cardura)

advantages:
rapid onset, safe, doesn’t alter PSa, symptoms improvemet maintained

SE: postural hypertension, retrograde ejaculation, headaches (maybe more)

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12
Q

formation, storage and release of thyroid hormones

A
  1. iodide topping (active transport from blood into cytosol by Na+/I- cotransport)
  2. synthesis of thyroglobulin (in RER, modified in Golgi complex and packaged into secretory vesicles) and exocytosis into follicular lumen
  3. oxidation of iodide: 2I- –> I2 and pass into follicle lumen
  4. iodination of tyrosine: T1 or T2 –> TGB + iodine atoms = colloid
  5. coupling of T1 and T2: T3 or T4
  6. Pinocytosis and digestion of colloid: merge with lysosomes in follicular cells : digestive enzymes break down TGB and cleave T3/T4
  7. secretion of thyroid hormones: diffusion into blood (lipid soluble)
  8. transport in blood: combine wit TBG (thyroxine-binding globulin)
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13
Q

actions of thyroid hormones

A
  1. increase basal metabolic rate: stimulate use of cellular oxygen to produce ATP: increase of metabolism of carbohydrates, lipids and proteins
  2. additional Na+/K+ ATPases synthesis: calorinergic effect (increase use of ATP and more heat produced)
  3. stimulation of protein synthesis + increase use of fatty acids and glucose (for ATP) + stimulates lipolysis, cholesterol excretion
  4. up regulation of beta receptors: increase HR, BP
  5. accelerate body growth, especially nervous and skeletal systems
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14
Q

what is basal metabolic rate

A

rate of oxygen consumption under standard or basal conditions (awake, at rest and fasting)

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15
Q

control of thyroid hormone secretion

A
  1. low blood levels of T3(/T4) or low metabolic rate stimulate hypothalamus to secrete TRH
  2. TRH stimulates thyrotrophs to secrete TSH (in pituitary gland)
  3. TSH stimulates all aspects of thyroid follicular cell function
  4. thyroid gland release T3 and T4
  5. elevated T3: negative feedback inhibition of TRH and TSH
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16
Q

calcitonin production: where and how, actions

A

parafollicular cells
high levels of Ca2+ stimulates calcitonin (controlled by neg feedback)
inhibits osteoclasts activity (bone resorption): decrease blood calcium and phosphate levels

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17
Q

effect of parathyroid hormone on bone

A

increase number and activity of osteoclasts: increase bone resorption: increase Ca2+ and HPO42- (phosphate) release in blood

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18
Q

effect of parathyroid hormone on kidney

A
  1. slows rate that Calcium and magnesium are lost in urine
  2. increases loss of phosphate in urine
  3. promote calcitriol formation (active form of vit D): increase rate of calcium, phosphate and magnesium absorption in GIT
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19
Q

adrenal glands structure

A

adrenal cortex: zona glomerulus, fasciculata, reticular

adrenal medulla

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20
Q

secretions of adrenal cortex and adrenal medulla

A

zona glomerulus: mineralicorticoids
zona fasciculata: glucocorticoids
zona reticularis: androgens
adrenal medulla: noradrenaline and adrenaline

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21
Q

thyroid hormone receptors

A
  • TR alpha 1 and 2
  • TR beta 1 and 2

TR alpha 2 does not bind T3 (the rest of the receptors binds with more affinity to T3)
TR beta 2 only found in the brain (the rest are found throughout the body)

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22
Q

cellular action of thyroid hormones

A
  • thyroid hormones receptors found in nucleus (form dimers either between 2 hormone receptors or with retinoid acid receptor)
  • in absence if thyroid hormone, TR receptor binds to DNA and represses gene transcription (with co-repressor), in presence of thyroid hormone, co-repressors replaces by co-activators: gene transcription activated
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23
Q

bodily effects of thyroid hormone

A

cardiovascular: increased cardiac output, increase HR and stroke volume, decreased systemic vascular resistance, increased systolic pressure

metabolic effects: increase BMR, increased oxygen consumption, increased thermogenesis, increased protein turnover

neurological effects: enhances wakefulness, memory, alertness, reflexes, normal emotional tone

growth and development: fatal growth neural development, normal bone growth and birth, normal tooth development

Reproduction: essential for normal reproductive function

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24
Q

propanolol

A

beta blocker:

use: ischemic heart disease, chronic heart failure, atrial fibrillation, supra ventricular tachycardia, hypertension

MOA: reduce force of contraction and speed of conducting in the heart (block beta1 adrenoreceptors)

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25
Q

what enzyme deiodinates T4 to T3

A

iodinase

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26
Q

action of thyroid peroxidase (TPO)

A

iodide ions to iodine atoms

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27
Q

MOA of carbimazole

A

inhibit TPO

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28
Q

MOA of propylthiouracil

A

inhibits TPO + stops conversion from T4 to T3

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29
Q

blood supply of kidney

A

renal artery –> segmental –> interlober –> arcuate –> cortical radiate –> afferent arteriole –> glomerulus –> efferent arteriole –> peritubular capillaries/vasa recta –> cortical radiate vein –> arcuate –> interlobal –> segmental –> renal

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30
Q

three layers of glomerulus

A
  • endothelium
  • basement membrane
  • podocytes
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31
Q

charge barrier of glomerulus

A

glycocalyx (heparin sulfate)

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32
Q

auto regulation mechanisms of kidney

A
  • myogenic

- tubuloglomerular feedback

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33
Q

how do you measure GFR (renal clearance)

A

volume of plasma which is cleared of substance x per uni of time: (urinary concentration of x * urine volume per unit time)/ plasma concentration of x

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34
Q

how much sodium reabsorbed in different parts of nephron

A

PCT: 67%
loop of Henle: 25%
DCT and CD: 8%

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35
Q

what are the four processes of Motivational Interviewing?

A
  • engaging
  • focussing
  • evoking
  • planning
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36
Q

how do you measure proteinuria?

A
  • PCR (protein:creatinine ratio)

- ACR (albumin:creatinine ratio)

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37
Q

stages of injury of diabetic nephropathy

A 
hyperfiltration
microalbuminuria
macroalbuminuria
proteinuria 
declining renal function
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38
Q

pathology of diabetic nephropathy

A 
-glomerular:
GBM thickening
mesangial cell expansion
nodular sclerosis
advanced sclerosis
  • tbulo-interstitial
  • vascular
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39
Q

treatment goals for diabetic nephropathy

A

-glycaemic control
-BP control
-RAAS bockade
-lipid lowering
-reduce other CV risks
(SGLT2 inhibitors)

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40
Q

renal replacement therapy

A

peritoneal dialysis
haemodialysis dialysis
haemofiltration dialysis
transplant

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41
Q

pathogenesis of viral hepatitis

A

non-cytopathic virus:

  • immune-mediated hepatocyte damage
  • Ag recognition by cytotoxic T cells causing apoptosis
  • hemokine driven recruitment by Ag-non-specific cells
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42
Q

which hep is only acute

A

hep A

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43
Q

when do you define hepatitis as chronic

A

persistence of infection > 6 months

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44
Q

hep A virus

  • name/types
  • incubation period
  • complications
  • diagnosis
A 
-RNA virus
picornavirus
-30 days (4-6 weeks)
- prolonged cholestasis, liver failure
-acute infection HAV IgM, recovery/vaccination: HAV IgG
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45
Q

hep E virus

  • name/types
  • incubation period
  • genotypes
  • complications
  • diagnosis
A
  • RNA virus herpevirus
  • 40 days
  • genotype 1,2 waterborne outbreaks, genotype 3,4 zoonotic
  • higher mortality in cirrhotics, pregnant women, acute neurological syndromes, type 3, 4 can become chronic in immunosuppressed patients
  • HEV IgM (Hep E IgG, HEV RNA blood, stool)
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46
Q

hep B virus

  • name/types
  • incubation period
  • complications
  • diagnosis
  • treatment
A
  • DNA virus (hepadnaviridae)
  • 75 days (6 weeks to 6 months)
  • end stage liver disease (cycles of inflammation and repair lead to fibrosis) and liver cancer
  • HBsAg, core Ab: chronic infection, core Ab: previous exposure
  • interferon, tenofovir, entecavir
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47
Q

hep Delta virus

  • name/types
  • infections routes
  • complications
  • diagnosis
  • treatment
A
  • defective RNA virus (needs Hep B to replicate)
  • blood, sexual: simultaneous or superinfection with HBV (uses surface antigen for enveloppe)
  • severe hepatitis, cirrhosis, hepatocelullar carcinoma
  • hep delat IgM, IgG, HDV RNA
  • PEG IFN
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48
Q

hep C virus

  • name/types
  • incubation period
  • complications
  • diagnosis
  • treatment
A
  • RNA Flavivirus
  • 2 weeks- 6 months
  • chronic infection
  • HCV Ab pos and HCV RNA pos: chronic infection, HCV Ab pos and HCV RNA neg: prior exposure
  • treatable because life cycle takes place in cytoplasm (no viral reservoirs)
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49
Q

liver zone 1

A

periportal

  • aa catabolism
  • gluconeogenesis
  • cholesterol synthesis

–> requires a lot of oxygen

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50
Q

liver zone 3

A

pericentral

  • lipid synthesis
  • ketogenesis
  • glutamine synthesis
  • drug metabolism
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51
Q

where does fibrosis start in the liver

A

zone 3

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52
Q

space between sinusoid and hepatocyte

A

space of Disse

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53
Q

bile composition

A
  • bile acids/salts (+phospholidpids and cholesterol)
  • bilirubin (conjugated)
  • metabolites of hormones and drugs
  • heavy metal ions
  • electrolytes (HCO3- and wate)
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54
Q

synthesis of bile acids/salts

A

cholesterol –> chalice acid –> (bacteria) deoxycholic acid + glycine (conjugated)

cholesterol–> chenodeoxycholic acid –> (bacteria) lithocholic acid + taurine (conjugated)

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55
Q

apical secretion of bile acids/salts transporters

A
  • BSEP (bile salt export pump)
  • MRP2 (multidrug resistance-associated protein 2)
  • -> both ABC transporters (ATP binding cassette)
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56
Q

lipid soluble bilirubin

A

unconjugated

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57
Q

where is conjugated bile salts absorbed in GIT and by which transporters

A

terminal ileum
ASBT (Na+ bile salt cotransporter
OST (organic transporter)

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58
Q

flippase action

A

maintains asymmetry in phospholipids on the outside and inside of cells: important for signalling

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59
Q

heme breakdown

A

heme –> (heme oxygenase)
biliverdin –> )biliverdin reductase)
bilirubin

by phagocytosis

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60
Q

bilirubin excretion

A

conjugated bilirubin –> (baceria) urobilinogen (unconjugated and colourless) –> stercobilin (brown or urobilin (yellow)

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61
Q

epithelial cells of bile duct

A

cholangiocytes

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62
Q

fluid secretion by cholngiocytes

A 
30-50% of hepatic bile
-secondary active transport of Cl- and HCO3-
-paracelular Na+ transport
-isosmotic water flow
(secreted by secretin, VIP and glucagon)
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63
Q

reabsorption by gall bladder epithelium

A
  • Na+ with NHE (secondary active transport)
  • Cl- reabsorbed for HCO3- + H+ secretion
  • isosmotic H20 absorption
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64
Q

bilirubin and drug binding to proteins

A

displaces it so more free drug

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65
Q

phases of metabolism of drugs

A

phase 1: functionalisation (produce/uncover chemically reactive functional groups i.e. oxidation): pharmacological activation
phase 2: conjugation (water soluble and easily excreted: pharmacological inactivation

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66
Q

CYP polymorphisms: different types of metabolisers and genes associated

A

poor (homozygous for defective gene)
intermediate (heterozygous for defective gene)
extensive (homozygous for functional gene)
ultra-rapid (extra copies of functional gene)

67
Q

paracetamol metabolism

A
  1. paracetamol –> glucuronide and sulphate conjugates of -OH group –> inactive metabolite
  2. paracetamol –> N-hydroxylation CYP450 –> re-arragemen: N-acetyl-p-benzoquinone imine –> glutathione conjugation –> inactive metabolite

(N-acetyl-p-benzoquinone mine can cause hepatotoxicity and cell death)

68
Q

illegal intoxication limit for alcohol

A

0.08 g/dL

69
Q

average elimination rate of alcohol

A

0.015 g/dL/hr

70
Q

non-alcoholic fatty liver disease

A
  • fatty change
  • non-alcoholic steatohepatitis (NASH)
  • fibrosis
  • cirrhosis
71
Q

cirrhosis what is is and causes and effects

A
  • disease of all the liver with parenchymal nodule and surrounding fibrosis
  • causes: alcohol, liver, metabolic diseases, autoimmune
  • effects: liver failure, portal hypertension and HCC
72
Q

what problems happen with liver failure?

A

protein synthesis: low albumin
coagulation factors: bleeding
jaundice
encephalopathy: confusion

73
Q

what problems happen with portal hypertension

A

ascites
varices
splenomegaly

74
Q

what signs with hepatocellular carcinoma

A

raised serum alpha-fetoprotein levels

75
Q

which organs sense glucose and what do they release

A
  • brain: sympathetic/parasympathetic
  • gut: incretins
  • beta cells: insulin
76
Q

ER stress on beta cells effect

A

protein misfolding and apoptotic cell death + accumulation of amyloid fibrils

77
Q

what are normal levels of fasting glucose and post prandial?

A

fasting: 4-<6 mol/L

post prandial <7.8 mmol/L

78
Q

gastroperesis and diabetes

A

slower gastric emptying: high levels of glucose can damage vagus nerve

79
Q

epsilon cells of pancreas production

A

gherlins: increase appette

80
Q

PP cells of pancreas production

A

pancreatic polypeptide: promote GI fluid secretion and satiety

81
Q

glycation

A

covalent bonding of a sugar molecule to a protein or lipid molecule (ie HbA1c)

82
Q

insulin receptor mechanism

A

2 insulin molecules binds to alpha chains leading to autophosphorylation of tyrosine kinase within beta chain: recruit adaptor proteins (i.e. insulin receptor substrate protein) with increases PI3K activity
–> insertion of GLUT in cell membrane

83
Q

incretins

  • names
  • function
A
  • GIP (glucose dependent insulinotropic polypeptide)
  • GLP-1 (glucagon like peptide-1)

functions: reduce glucagon secretion, increase insulin secretion, satiety, reduce glucose synthesis in liver, slow gastric emptying

84
Q

dysregulation of incretins in diabetes

A

GLP-1 secretion is reduced and sensitivity of beta cells to it is decreased
GIP response is reduced

85
Q

neuroglycopenia: what is in and when do you experience it

A

shortage of glucose in brain

at 3 mmol/L

86
Q

at what level of glucose do you experience sever neuoglycopenia?

A

1 mol/L

87
Q

treatment options for DM

A
  • insulin secratogogues: GLP-1 receptor antagonists, DPP4 inhibitors, sulphonylureas/meglitinides
  • insulin sensitisers: hiazolinadions, biguanides
  • decrease glucose reabsorption in kidney: SGLT2 inhibitors
  • slow glucose absorption: alpha-glucosidase inhibitors
88
Q

what is adiponectin

A

protein in adipocyte: insulin sentising and anti-atherogenic

89
Q

what is resistin

A

neutralising antibodies: reduce insulin resistance

90
Q

adipose tissue and IL6

A
  • correlation between IL6 and insulin resistance

- viscerl fat secretes 2x more IL6 than subcutaneous fat

91
Q

adipose tissue: endocrine release

A 
adiponectin
TNFalpha
Resisting
leptin
interleukin 6
92
Q

effects of leptin

A
  • muscle: increase glucose uptake and glycogenolysis
  • liver: decrease gluconeogenesis, increase glycogenolysis, increase beta oxidation
  • adipose: increase lipolysis, decrease lipogenesis
  • beta cells: decrease insulin synthesis and secretion
  • brain (hypothalamus): inhibition of feeding and increase of sympathetic output
93
Q

PPAR gamma activation effects

A

-increase adipogenesis –> decrease leptin and TNFalpha, increase FA disposal and glucose uptake –> increase insulin receptor function –>increase beta cell function and decrease HGO, glycogenolysis

94
Q

PPAR

what it stands for and what type of receptor

A

peroxidase Proliferator Activated Receptor

nuclear hormone receptor family, dimerises with retinoid X receptor (RXR)

95
Q

BMI values

A
  • 18.5-24.9: healthy weight
  • 25-29.9: overweight
  • 30-34.9: obesity 1
  • 35-39.9: obesity 2
  • +40: obesity 3
96
Q

body weight distribution names

A

gynaecoid: lower fat obesity (doesn’t have CV risks)
android: upper fat obesity

97
Q

insulin release from beta cell mechanism

A

glucose enters cell –> increase ATP which blocks K+ ATP channel –> incur intracellular ca2+ –> insulin exocytosis

98
Q

tests for DMT1 diagnosis

A
  • GAD antibodies
  • Islet cell antibodies
  • insulin antibodies
  • C peptide/Insulin/glucose levels
99
Q

treatment of DKA

A 
IV fluid
potassium replacement
insulin replacement
replacement of electrolytes
LMWH, antibiotics
100
Q

biguanides MOA

A

increase sensitivity to insulin

101
Q

thiazolidinediones MOA

A

insulin sensitiser: activated PPARgamma: increase insulin action

102
Q

example of TZD

A

pioglitazone

103
Q

example of sulphonylurease

A

glicazide

104
Q

DDP-4 inhibitors MOA

A

stimulate insulin and inhibit glucagon (glucose dependent)

105
Q

alpha 1 blockers examples

A

tamsulosin
alfuzosin
doxazosin

106
Q

what converts testosterone to dihydrotestosterone

A

5 alpha reductase

107
Q

example of 5 alpha reductase inhibitors

A

finasteride

dutasteride

108
Q

surgical options for prostate cancer

A

transurethral resection of prostate (TURP)

Holmium enucleation of prostate (HoLEP)

109
Q

red flags with the prostate

A 
urinary incontinence
renal impairement 
haematuria
recurrent urinary infections
raised PSA
110
Q

which nerves supply the bladder and with receptor/neurotransmitters associated

A
  • pelvic nerve (parasympathetic): ACh/M3 receptor (+)
  • hypogastric (sympathetic): NA/beta3 receptor (-) and in urethra: NA/alpha1 receptor (+)
  • pudental nerve (somatic): ACh/nicotinic receptor (+)
111
Q

three histological varieties in kidney malformation

A
  • hypoplasie (too few nephews)
  • dysplasia (undifferentiated kidney sometimes with cysts)
  • agenesis (absent kidneys)
112
Q

three histological varieties in kidney malformation

A
  • hypoplasia (too few nephews)
  • dysplasia (undifferentiated kidney sometimes with cysts)
  • agenesis (absent kidneys)
113
Q

renal coloboma syndrome

A

optic nerve malformation (blindness)
smal, malformed kidneys (kidney failure)
PAX2 transcription factor

114
Q

causes of acquired kidney failure

A
  • pre-renal causes: shock, cardia and liver failure
  • intrinsic kidney disease: glomerular and tubular disease
  • post-renal causes: urinary flow impairment
115
Q

different zones of the prostate

A

transitional zone
central (surrounding ejaculatory duct)
peripheral

116
Q

how many men are diagnosed with prostate cancer in the UK

A

1/8

117
Q

symptoms of prostate cancer

A

LUTS
metastatic (ie pain)
systemic (fatigue, weight loss)

118
Q

different types of prostate biopsy

A
  • transrectal ultrasound guided (TRUS) biopsy (through rectal wall with ultrasound)
  • template biopsy (transperineal)
119
Q

what scoring system do you use for prostate cancer

A

Gleason Score

score from 3-5 are considered cancerous

120
Q

action of TPO

A

thyroglobulin + I- –> thyroglobulin containing thyroid hormone (in coloid)

121
Q

which thyroid hormone has the longer half life

A

T4

122
Q

what can fT4 be turned into

A

T4 –> T4 –> rT3 or T3

123
Q

what can fT3 be turned into

A

T3 or T2

124
Q

What type of hormone is thyroid hormones

A

steroid

125
Q

where is T4 converted into T3

A

liver and kidney

126
Q

primary hypothyroidism aetiology

A
  • autoimmune thyroiditis
  • drugs (amiodarone, iodides, lithium)
  • iodide deficiency
  • congenital
  • post-ablative radioiodine/post-operative
127
Q

secondary/tertiary (hypopituitarism/hypothalamic) hypothyroidism aetiology

A
  • pituitary adenoma, congenital deficiency, irradiation

- sarcoid, infection

128
Q

investigations in hypothyroidism

A
  • thyroid function tets
  • nomochromic, normocytic anaemia
  • macrocytosis, mixed dyslipidaemia
  • increase serum AST, creatine kinase
  • hyponatremia
129
Q

aetiology of hyperthyroidism

A
  • Grave’s disease
  • toxic nodules
  • pituitary adenoma or thyroid resistance syndrome
  • trnasiet
  • pharmacological
130
Q

investigations primary hyperthyroidism

A
  • ultrasound: homogenous (Graves) or heterogenous (NMG)

- uptake sacan (homogenous or isolated ‘hot nodules’)

131
Q

treatment of hyperthyroidism

A

thionamide

radioiodine or surgery

132
Q

what are symptoms that are specific to Grave’s disease

A

all the hyperthyroidism symptoms +

  • tyroid eye disease/Graves orbitopathy
  • peritibial myxoedema
133
Q

What is Graves orbitopathy/thyroid eye disease

A

inflammation of extra ocular muscles: increase retro-orbital pressure –> proptosis
+ glycosaminoglycan deposits and fibrosis

134
Q

problems of pregnancy and Grave’s disease

A
  • spontaneous abortion
  • premature labour
  • small birth weight
  • congestive cardiac failure
  • pre-eclampsia
135
Q

HPA axis

A

circadian rhythm + stress –> (hypothalamus) CRH –> (anterior pituitary) ACTH –> (adrenal cortex) cortisol –> (neg feedback on hypothalamus and anterior pituitary)

136
Q

what is cortisol transformed into in the peripheral tissues

A

cortisone

137
Q

over production of mineralocorticoids syndrome

A

Conn syndrome

138
Q

over production of glucocorticoid syndrome

A

Cushing syndrome

139
Q

secondary adrenal gland under production cause and effect

A

hypopituitarism, loss of ACTH (aldosterone secretion preserved)

140
Q

what increase blood glucose levels

A

glucagon, catecholamines, cortisol, groth hormones

141
Q

drugs that prevent production of cortisol

A

metyrapone
ketoconazole
mitotane

142
Q

hormones that regulate BP

A
  • angiotensin 2
  • aldosterone
  • cortisol
  • catecholamines
  • calcium/PTH
  • growth hormones
143
Q

tumour of adrenal medulla

A

pheochromocytoma

144
Q

Addison’s diease

A

primary hypoadrenalism: decreased glucocorticoid, mineralocorticoid an sec steroid production

145
Q

(EBM) what is odds

A

likelihood of an event/outcome occuring

146
Q

how do you calculate odds

A

nb of individual with outcome/nb of individuals without outcome

147
Q

in regards to odds, when is an event more likely to happen than not

A

when greater than 1

148
Q

when odds ratio (relative odds) used?

A

used to compare whether likelihood of certain event occurring is same for row groups

149
Q

how do you calculate odds ratio?

A

odds of outcome in one group/odds of outcome other group

150
Q

fat soluble vitamin absorption

A

facilitated diffusion and/or endocytosis

151
Q

water soluble vitamins names

A

B and C

152
Q

water soluble vitamins absorption

A 
specific transporters (facilitated and secondary)
B12 by endocytosis
153
Q

what are the two types of Chi-square tests

A

goodness of fit

test of independence

154
Q

what does the goodness of fit Chi square test test

A

observed frequency distribution differs from theoretical distribution

155
Q

what does the test of independence Chi square test test

A

paired observation on two variables expressed in a contingency table, are independent of each other

156
Q

what does false negative and false positive mean

A

false positive: have positive result but don’t actually have the disease
false negative: have negative results but actually have disease

157
Q

what is sensitivity (EBM)

A

probability of correctly diagnosing a condition (true positives)

158
Q

what is specificity

A

probability of correctly identifying a non-disease person (true negatives)

159
Q

how do you calculate sensitivity

A

true positives/ (true positives+ false negatives)

160
Q

how do you calculate specificity

A

true negatives/ (true negatives + false positives)

161
Q

what is the positive predictive value

A

probability that disease is present when test is positive

162
Q

how do you calculate the positive predictive value?

A

true positives/ (true positives + false positives)

163
Q

what is the negative predictive value?

A

probability that the disease is not present when the test is negative

164
Q

how do you calculate the negative predictive value

A

true negatives / (false negatives + true negatives)

sem 4 (2 decks)

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