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General medicine > Gastroenterology > Flashcards

Gastroenterology Flashcards

1
Q

Girotra’s trait: what does it indicate?

A

Clostridium difficille infection

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2
Q

C. diff: what does it cause?

A

Pseudomembranous colitis

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3
Q

C. diff: what bacteria is it?

A

gram +ve

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4
Q

Girotra’s triad of c.diff: features

A

increased pain/distention and diarrhoea
leukocytosis >18k
haemodynamic instability

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5
Q

C. diff infection treamtment

A

stop causative abx
metronidazole or vancomycin for up to 10d
urgent colectomy for toxic megacolon

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6
Q

Acute severe diarrhoea: management

A

treat cause
rehydrate: IV saline + 20 mmol K+
codeine phosphate (antimotility drug/opioid receptor)
loperamide (antimotility/ opioid r. but doesn’t cross BBB)
avoid abx unless injective

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7
Q

CIrrhosis: define

A

irreversive liver damage

loss of architecture with bridging fibrosis and nodular regeneration

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8
Q

Cirrohosis: complications:

A

liver failure
portal hypertension
hepatocellular carcinoma (HCC) increased risk

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9
Q

Hereditary Haemochromatosis define

A

disorder of iron metabolism
increased iron absorption
causes liver deposition in the joints, liver, heart, pancreas, pituitary, adrenals and skin

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10
Q

Hereditary Haemochromatosis: signs

A

early: none or tiredness, arthralgia (pseudo-gout)
later: slate-grey pigmentation of the skin, chronic liver disease signs, osteoporosis
Endocrinopathies: DM, hypogonadism (putuitary deposits)

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11
Q

alpha-1 antitripsin deficiency: cause and effects

A

inherited disease in serine protease inhibitor, mechanism unclear
it controls inflammation
affects the lungs (emphysema) and liver (cirrhosis and HCC)
causes liver disease in children (cholestatic jaundice)

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12
Q

WIlson’s disease: define

A

autosomal recessive inherited disorder of biliary copper excretion (problem with copper incorporation in hepatocytes and its excretion into bile)

  • > too much copper in liver and CNS (basal ganglia)
  • > screen young in cirrhosis
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13
Q

Cirrhosis: signs

A

leuconychia (hypoalbuminaemia), Terry’s nails (Talangectesia distally),clubbing
palmar erythema, Dupuryen’s circulation
hyperdynamic circulation
spider naevi, xanthelasma,
hepato- and spleno- megally/small liver
Portal HTN: astices, splenomeg, varices, caput metusae

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14
Q

Cirrhosis: management

A 
nutrition, avoid alcohol, NSAIDs, sedatives and opiates
colestyramine for pruritus 
consider USS +/- alpha fetoprotein 
varicies-> banding 
recurrent encephalopathy-> rifaximin
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15
Q

Cirrhosis: diagnosis

A

transient elastography in pt’s at risk
biopsy if unsuitable
caution in obese or T2DM
re-test high risk patients every 2 yrs

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16
Q

Recurrent encephalopathy management

A

rifaximin

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17
Q

Primary biliary cirrhosis: define

A

interlobular bile ducts damage by chronic autoimmune gronulomatous inflammation (genetic and environmental influence)
-> cholestasis
-> fibrosis, cirrhosis and portal HTN
hallmark: antimitochondial antibodies (AMAs)
malabsorption of fat soluble vitamins (due to cholestasis and inc bilirubin)

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18
Q

Primary sclerosing cholangitis: define

A

progressive cholestatis with bile duct inflammation and strictures (outside of liver)
-> pruritis +/- fatigue
-> ascending cholangitis, cirrhosis and end-stage liver failure
primary or secondary to infections, thrombosis or trauma

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19
Q

Liver failure: signs

A

jaundice, encephalopathy
pear drop smell
liver flap (asterixis)
constructional apraxia (Star)

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20
Q

Liver failure: investigations

A

FBC, U&E (use creatine for renal func.), LFT, clotting (inc. prothrombin, INR), paracetamol levels
blood/urine culture, ascitic tap (MC&S)-> spontaneous bacterial peritonitis
CXR, abdo USS, Doppler portal v. (Budd-Chiari synd)

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21
Q

Budd-Chirari syndrome: define

A

hepatic vein obstruction by thrombosis or tumour

  • > ischaemia and hepatocyte damage
  • > abdo pain, hepatomegaly, ascites and inc. ALT
  • > portal HTN in chronic cases
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22
Q

Liver failure management

A

ITU bed 20* head up tilt
Protect airway (intubation + NG to for aspiration risk and remove blood from stomach)
Fluid status (urinary and central venous catheters)
Obs + daily weights
FBC, U&E, LFT and INR daily
avoid hypoglycaemia (frequent BMs +/- 10% dextrose IVI)
Nutrition (thiamine and folate supplements)
Lorazepam for seizures
Consider liver transplant

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23
Q

Hepatic encephalopathy: pathophysiology

A

liver failing -> amonia waste builds up in curculation

  • > passess to the brain
  • > cleared by astrocytes (glutamate-> glutamine)
  • > glutamine builds up
  • > osmotic imbalance
  • > cerebral oedema
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24
Q

Hepatic encephalopathy: stages

A
  1. altered mood/behaviour (sleep disturbance, dyspraxia (star), no liver flap)
  2. Increased drowsiness, confusion, slurred speech, liver flap, inappropriate behaviour and personality change
  3. Incoherent, restless, liver flap, stupor
  4. coma
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25
Q

Liver transplant indications

A

end stage liver failure (acute or chronic)

primary liver cancers

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26
Q

Liver transplant donation options

A

living donor: right lobe (for critically ill)

cadeveric donor

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27
Q

Hepatorenal syndrome: define and pathophysiology

A

cirrhosis, ascites and renal failure (abnormal haemodynamics)
bacterial translocation cytokines and mesenteric autoregulation
-> splanchnic and systemic vasodilatation
-> renal vasoconstrictio

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28
Q

Hepatorenal syndrome: types

A
  1. rapidly progressive, <2wks median survival -> Terlipressin and haemodialysis may be needed
  2. steady deterioration, survival around 6 months. Transjugular intrahepatic potrosystemic shunt
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29
Q

Jaundice: pathophysiology (from haemoglobin breakdown)

A

Hb broken down to Heme and globin.
Heme is converted to UCB by heme oxygenase (bound to Albumin as water insoluble)
Enters the liver where it gets unbound
UCB+ glucoronic acid -> CB excreted in bile enters the intestine
bacteria cleave glucoronic acid off and CB -> Urobilinogen
Excteted in urine (10%) and in faeces (90%- steobilin)

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30
Q

What happends to globin after Hb breakdown?

A

Broken down by macrophages of the reticuloendothelial system (Kupffer cells)

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31
Q

Pre- hepatic jaundice UCB and CB levels, urine and stool colour

A

UCB- increased
CB- normal
urine- normal
stool- normal

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32
Q

Hepatic jaundice UCB and CB levels, urine and stool colour

A

UCB- increased
CB- increased
urine- dark
stool- normal

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33
Q

Post- hepatic UCB and CB levels, urine and stool colour

A

UCB- normal
CB- increased
urine- dark
stool- pale (low levels reach the intestine due to an obstruction)

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34
Q

Kernicterus: define

A

unbound bilirubin deposited in infant basal ganglia

-> bilirubin induced brain dysfunction

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35
Q

Causes of acute jaundice in cirrhosis patient

A

sepsis
malignancy
alcohol and drugs
GI bleeding

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36
Q

Hereditary Haemochromatosis: management

A

venesection

consider vitamin supplements

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37
Q

Primary sclerosing cholangitis: associated cancers

A

increased risk of bile duct, GB, liver and colon cancer

-> yearly colonoscopy and USS

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38
Q

Hepatitis A: pathogen type and course

A

RNA virus

self limiting and not chronic

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39
Q

Hepatitis A: incubation time and symptoms

A

2-6 wks

fever,malaise, anorexia nausea, arthralgia, jaundice, hepato and splenomegaly and adenopathy

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40
Q

Hepatitis A: investigations

A

ALT ^^
AST ^
IgG detectable for life
IgM for 20d to 20wks

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41
Q

Hepatitis A: management

A

immunization (harvix monodose)-> for 1 year

usually self- limiting

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42
Q

Hepatitis B: pathogen type

A

DNA virus

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43
Q

Hepatitis A: spread

A

faecal-oral route

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44
Q

Hepatitis B: spread

A

blood products, IV drug use, sexual, direct

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45
Q

Hepatitis B: incubation time and symptoms

A

1-6 months

fever, malaise, anorexia, nausea, arthralgia and uratica, jaundice

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46
Q

Hepatitis B: investigations

A

HBsAg (surface antigen, if +ve over 6m -> carrier)

HBeAg (antigen, +ve during acute phase and up to 3 m after) -> implies increased infectivity

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47
Q

Hepatitis B: management

A

vaccination (specific anti-HBV immuniglobulin) for high risk exposure individuals
avoid alcohol
antivirals: PEG intaferon alpha 2a, lamivudine, entecavir, adefovir

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48
Q

Hepatitis C: pathogen type

A

RNA flavivirus

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49
Q

Hepatitis C: spread

A

blood transfusion, IV drug use, sexual, acupuncture

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50
Q

Hepatitis C: course

A

early infection often mild or asymptomatic

  • > 85% silent chronic infection
  • > 25% cirrhosis -> 4% HCC
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51
Q

What’s the commonest cause of liver transplant?

A

Hep C

52
Q

Hepatitis C: investigations

A

LFT- AST:ALT <1:1 until cirrhosis develops
HCV PCR confirms diagnosis, if +ve:
-biopsy to check liver damage and need for Rx
-HCV genotype
- viral load

53
Q

Hepatitis C: management

A

boceprevir
telaprevir (both serine protease inhibitors)
PEG interferon alpha 2a

54
Q

Autoimmune hepatitis: define

A

liver inflammation without a known cause

characterised by T-cell defects with autoantibodies against hepatocyte surface agents

55
Q

Autoimmune hepatitis: investigations

A

increased bilirubin, alk phos, ALT, AST
inc. IgG
+ve antibodies: ANA, ASMA, LKM1, SLA (variable depending on the type)

56
Q

Autoimmune hepatitis: management

A

immunosuppression (prednisolone min. 2yrs and/or Azathrioprine)
liver transplant for decompensated cirrhosis or unsuccesful medical treatment

57
Q

Wilson’s disease: clinical features

A

liver disease (Esp. in young)
CNS signs: tremor, dyarthria etc
mood: depression/mania, personality change
cognition: memory loss, IQ deterioration, delusions, mutism, irritability
Kayser-Fleischer rings (iris)
haemolysis

58
Q

Wilson’s disease: investigations

A 
24h urine copper collection 
non specific LFT increase 
decreased serum copper 
decreased coeruplasmin (but can be low in low protein states)
molecular genetic testing 
liver biopsy: inc. copper
MRI: basal ganglia deterioration
59
Q

Wilson’s disease: management

A

diet: avoid copper high meals
panicillamine (chelating agent) lifelong
liver transplant
screen siblings

60
Q

Chronic liver disease pt: Haemochromatosis screen

A

iron studies (increased iron, inc ferrin, inc total iron binding capacity

61
Q

Chronic liver disease pt: alpha 1 antitrypsin def. screen

A

A1AT levels + genotyping

62
Q

Chronic liver disease pt: Wilson’s disease

A

low copper and caeruloplasmin

63
Q

Chronic liver disease pt: Primary biliary cirrhosis

A

AMA antibodies

64
Q

Chronic liver disease pt: Primary sclerosing cholangitis

A

ANA, SMA and ANCA may be increased (but AMA negative)

65
Q

Chronic liver disease pt: autoimmune hep

A

increased ANA, ASMA, IgG

66
Q

Chronic liver disease pt: HCC

A

alpha fetoprotein

67
Q

Chronic liver disease pt: Gilbert’s disease

A

increased bilirubin concentration with normal LFTs

68
Q

IBS management: constipation

A

bisacodyl, sodium picosulfate and ispaghula

69
Q

IBS management: diarrhoea

A

bulking agents +/- loperamide

avoid sorbitrol in sweateners

70
Q

IBS management: colic/bloating

A

mebeverine, alverine citrate, dicycloverine

71
Q

IBS management: psychological symptoms meds

A

anticyclics: amitryptyline

72
Q

Pt with diarrhoea and weight loss/anorexia; suspect

A

coeliac disease

73
Q

Coeliac disease: define

A

t-cell mediated autoimmune disease of the small bowel
prolamin (gluten- alcohol soluble proteins in wheat, barley, rye +/- oats) intolerance
-> villous artophy and malabsorption (inc bile acids)

74
Q

Coeliac disease: investiagtions

A

low Hb, ferrin, B12
increased RCDW (Red cell distribution width)
serological testing: inc total IgA and IgA tissue transglutaminase. if inconclusive -> IgA EMA

75
Q

Coeliac disease: biopsy results

A

duodenal biopsy
subtotal villous atrophy
intra epithelial WBC
crypt hyperplasia

76
Q

Coeliac disease: complications

A 
anaemia 
2* lactate intolerance 
GI t-cell lymphom a
increased risk of malignancy 
myopathies 
hyposplenism 
osteoporosis
77
Q

Coeliac disease: associated skin condition

A

dermatitis hypetiformis

78
Q

Diabetes: cardiovascular risk assessment

A

QRISK2
- age, gender, smoking, diabetes, angina/MI/1st degree relative, HTN Rx, postcode, BMI, systolic BP, total and HDL cholesterol, ethnicity

79
Q

Diabetes: diagnosis

A

symptoms of hypergylcaemia (polyuria, polydipsia, unexplained weight loss, visual blurring) and
increased venous glucose (7+ fasting or 11.1+ random)
or increased on 2 separate occasions
or HbA1C 6.5% +

80
Q

Diabetes: treatment options

A 
Metformin 
Sulfonylurea 
Glitazone
GLP1 analogues and DPP4 
Insulin
81
Q

Diabetic ketoacidosis: define

A

acidaemia, hyperglycaemia, ketoanaemia
life-threatening.
venous XS glucose due to lack of insulin

82
Q

Diabetic ketoacidosis: management

A

IV fluids
insulin infusion: atrapid
K+ status: low -> potassium phosphate/chloride
or high -> calcium gluconate, salbutamol

83
Q

Diabetes: HONK diagnosis

A

hyperglycaemic hyperosmolar non-ketotitc coma

+/- decreased conscious level and mental confusion

84
Q

Diabetes: HONK management

A 
slow rehydration (6-12 l may be required)
insulin infusion (actrapid)
NG tube (unconscious) 
LMWH
85
Q

Causes of hypoglycaemia

A

ExPLAIN
Exogenous drugs (insulin, hypoglycaemic drugs)
Pituitary insufficiency
Liver failure
Addison’s disease
Islet cell tumours/ Immune hypoglycaemia (Hodgkin’s disease(
Non-pancreatic neoplasms

86
Q

Hypoglycaemia: management

A

20-30g glucose IV or
glucagon (not in drunks)
if conscious: sugary drink and a meal

87
Q

Microvascular complications of diabetes

A

retinopathy
nephropathy
neuropathy

88
Q

Diabetic retinopathy stages and features

A

background retinopathy: microaneurysms, haemorrhages and hard exudates
pre-proliferative: cotton wool spots, haemorrhages, venous bleeding (Retinal ischaemia)
proliferative: new vessel formation
maculopathy: reduced acuity (changes as above)

89
Q

Diabetic retinopathy: pathogenesis

A

capillary basement membrane thickening -> leaky vessels, lipid deposids

90
Q

Diabetic retinopathy: when to refer

A

pre-proliferative stage
changes near the macula
(annual eye checks)

91
Q

Diabetic nephopathy: pathophysiology

A

glomerular hyperfiltration initially
GBM thickening -> eGFR decreases
microalbuminaemia
-> HRN, oedema and uraemia

92
Q

Diabetic neuropathy: pathophysiology

A

damage to small blood vessels supplying the nerves and abnormal sugar metabolism
-> peripheral sensory neuropathy (loss of vibration sense and glove and stocking distribution of neuropathy)

93
Q

Diabetic neuropathy: deformities

A 
pes cavus, claw toes, loss of transverse arch, rocker-bottom sole 
bony deformity- Charcot's deformity 
foot ulceration (punched out painless)
94
Q

Diabetes: macrovascular complications

A

atherosclerosis

foot disease -> ulceration, gangrene

95
Q

Cause of primary hyperlipidaemia

A

Account for 70% of cases

- familial primary hyperlipidaemia (multiple phenotypes)

96
Q

Causes of secondary hyperlipidaemia

A 
Cushing's syndrome 
hypothyrodism 
nephrotic syndrome 
cholestasis 
Mixed hyperlipidaemias: T2DM, metabolic syndrome, alcohol abuse, CKD
97
Q

Hyperlipidaemia: managmenet

A

Diet (reduce saturated fats), weight loss
treat known CVD, DM and 10 year risk of CVD >20%
(target plasma cholesterol 4 mmol/l or less)
-> statins
-> fibrates

98
Q

Posterior pituitary: features

A

collection of axonal (large diameter) projections from the hypothylamus containing nerve endings (Start in the supraopic and paraventricular nuclei)

99
Q

Posterior pituitary: hormones produced and function

A

ADH-> water balance regulation, increased water permeability in the distal convoluted tubule (Aquaporin 2 insertion in the basolateral membrane)
OXYTOCIN -> uterine contraction and lactation

100
Q

Anterior pituitary: features

A

glandular tissue synthesis and secretes 5 peptide hormones

under the control of hypothylamic releasing hormones transported in the hypophyseal portal veins

101
Q

Anterior pituitary: hormones produced

A 
ACTH 
TSH
FHS
LH
Growth hormone 
Prolactin
102
Q

Test for primary adrenal failure

A

syntacthen test

  • no response -> adrenal problem
  • normal response excludes Addison’s
103
Q

Test for hypopituatarism

A

insulin tolerance test
- tests ACTH and growth hormone reserve
differentiates between normal individual from ACTH deficiency
(Stress -> cortisol needed, ACTH should be released)

104
Q

Test for acromegaly

A

glucose tolerance test
stress/hypoglycaema -> growth hormone
bolus glucose -? suppression of growth hormne in a normal person
acromegaly- failure to suppress

105
Q

Test for Cushing’s syndrome

A

Dexamthasone suppression test
Potent supressor of cortisol release
no suppression- ectopic ACTH/Cortisol release
suppression- confirms Cushing’s syndrome

106
Q

Pituitary tumours: clinical features (local)

A

visual loss- bitemporal heminopia (optic chiasm compression) + red. visual acuity
pituitary failure/hypopituatirism
general: headaches, diplopia

107
Q

Pituitary tumours: types

A

micoadenomas vs macroadenomas

functioning vs non-functioning

108
Q

Hypopituatirism: hormone levels

A

all decrease except for prolactin, which increases (under inhibatory control from dopamine)
panhypopituitarism if all hormones affected

109
Q

Hypopituitarism: causes

A

hypothalamus: kallman’s synd, tumour, inflamm., infection, ischaemia
pituitary stalk: trauma, surgery, mass, menangioma, carotid artery aneurysm
pituitary gland: tumour, irradiation, inflammation, autoimmune, infiltration (Amyloid, haemochromatosis, mets) or ischaemia

110
Q

Hypothalamus- thyroid axis

A

Hypothalamus -> TRH
Anterior pituitary -> TSH
Thyroid gland -> T3 and T4 (negative feedback)

111
Q

Hypothyrodism: differentiation between primary and secondary

A

primary: increased TSH and decreased T4
secondary: low or normal TSH (problem in the pituitary)

112
Q

Hypothyrodism: treatment

A

levothyroxine

113
Q

Hyperthyrodism: causes

A

Grave’s disease (2/3 cases)
toxic multinodular goitre (15%)- in eldery and iodine deficient -> xs secretion w/o stimulation
Toxic adenoma producting T3/4 with the rest of the gland suppressed by XS TSH
Ectopic thyroid tissue

114
Q

Hyperthyrodism: management

A

B-blockers for symptoms
carbimazole
radioiodine
thyroidectomy

115
Q

Cushing’s syndrome; ACTH dependant causes (3)

A

Cushing’s disease: bilateral adrenal hyperplasia from ACTH secreating pituitary adenoma
Ectopic ACTH production (non-pituitary, eg small cell carcenoma)
Ectopic CRH production (rare) from thyroid and prostate cancers

116
Q

Cushing’s syndrome: ACTH independent cause

A

ACTH is low due to -ve feedback
adrenal adenoma/cancer
Iatrogenic- steroids
Adrenal nodular hyperplasia

117
Q

Metabolic syndrome: define

A

central obesity (BMI >30 or increased weist) + 2 of the following:

  • BP 130/85 or higher
  • trygliccerides 1.7mmol/l or more
  • HDL low
  • fasting glucose 5.6mmol or more or DM
118
Q

Craniopharyngioma: define

A

Rathke’s pouch tumout (not pituitary)
commonest childhood intracranial tumour
-> growth failure
adults -> ammenorrhoea, reduced libido, hypothalamic symptoms or tumour mass effect

119
Q

Adrenal gland structure and hormones produced

A 
Cortex:
- z. glomerulosa -> mineralocorticoids 
- z. fasciculata -> glucocorticoids 
- z. reticularis -> adrogens 
Medulla -> catecholamines (Na and adrenaline)
120
Q

Addison’s disease: define

A

Primary adrenocortical failure

121
Q

Addison’s disease: treatment

A

replace steroids
mineralocorticoids to correct postural HTN
avoid abrupt stopping of steroids

122
Q

Endocrine HTN: causes

A

hyperaldosteronism (primary: Conn’s syndrome or secondary to adrenal hyperplasia )
phaeochromocytoma

123
Q

AKI stages

A
  1. creatine 1.5x baseline or <0.5 ml/kg/h urine output in 6 hours
  2. C 2x baseline or <0.5 ml/kg/h urine output in 12h
  3. X 3x baseline (or >354micromol/l) or <0.3 ml.kg.h output in 24 h or anuria for 12
124
Q

Uteric calculi treatment

A 
nephrostomy tube placement, insertion of ureteric catheters or ureteric stent placement. 
shock wave lithotripsy, 
percutaneous nephrolithotomy, 
ureteroscopy, 
open surgery
125
Q

What type of anaemia is present in Haemolytic uraemic syndrome and Thrombotic Thrombocytopenic purpura?

A

Microangiopathic haemolytic anaemia (MAHA)

General medicine (2 decks)

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