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Finals > Hepatology, endocrinology, renal > Flashcards

Hepatology, endocrinology, renal Flashcards

1
Q

3 ways alcoholic liver disease affects liver

A

Hepatic steatosis (also obesity and DM) - alcohol metabolism prioritised, so fat not metabolised and accumulates in cytoplasm of liver cells
Alcoholic hepatitis - direct toxicity, collagen deposition, cirrhosis
Cirrhosis - final and irreversible. Hepatocytes regenerate with nodules and fibrous septa - blood flow disrupted and less efficient

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2
Q

Assoc of non alcoholic fatty liver diseae

A

Metaboic syndrome, insuin resistance

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3
Q

RF for NAFLD and sx

A

Obesity, diabetes, hyperlipidaemia

Asymptomatic of fatigue and malaise

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4
Q

Sx of alcoholic hepatitis

A

Anorexia, dv, tender hepatomegaly, ascites

Jaundice, bleeding, encephalopathy

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5
Q

Inv for alc hep

A

Raised MCV
Raised GGT
AST:ALT >2
Ascitic tap, abdo USS, portovenus duplex

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6
Q

Manage alc hep

A 
Stop alcohol and drug withdrawal 
High dose vit B
Optimise nutrition
Daily weights
LFT, UE, INR
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7
Q

Signs of chronic liver failure

A 
Jaundice, oedema, ascites
Bruising
Encephalopathy - asterexis, constructional apraxia
Fetor hepaticus
Signs of cirrhosis
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8
Q

Manage chronic liver failure

A

ITU
Thiamine supplements
Prophylactic PPI for stress ulcers

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9
Q

Manage complications of chronc liver failure

A

Bleeding - Vit K, platelets, ffp, blood
Ascites - fluid and salt retention, spironolactone, furosemide, ascitic tap, daily weighing
Hypoglycaemia - regular BMs, IV glucose if <2
Sepsis - tazocin
Encephalopathy - avoid sedatives. Give lactulose/enemas, rifaximin
Seizures - lorazepam
Cerebral oedema - mannitol

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10
Q

Poor prognostic factors for chronic liver failure

A

Grade 3-4 hep encephalopathy
>40yo
Low albumin, raised INR
Drug induced

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11
Q

What is hepatic encephalopathy

A

Neuro disorder from 1) metabolic failure of hepatocytes and 2) blood shunting around liver - exposes brain to abn metabolites = oedema and astrocyte changes
Elimination of toxic nitrogenous products reduced and some act as false transmitters causing CNS disturbances

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12
Q

Sx of hep enceph

A

Disturbance of consciousness
Flapping tremor
Fluctuating neuro signs - muscular rigidly and hyperreflexia

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13
Q

Conditions where liver transplantation is used - 5

A 
Acute and chronic liver disease
Alcoholic liverdiseae
PBC
Chronic hep b/c with complications 
Primary metaoblic disease with endstage liver diseae eg Wilson’s, a1at
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14
Q

Absolute CI to liver transpant

A

Sepsis out]side hepbil tree, malignancy

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15
Q

Signs of rejection in liver transplant and manage

A

Early 5-10d = inflammatory reaction = pyrexia, general malaise, abdo tenderness from hepmeg
Give immunosuppression post transplant - Calcineurin inhibitor, steroids, azathioprine
Chronic - 6w-9m after - immunosuppression and retransplant

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16
Q

Manage ascites before liver transplant

A

Oral ciprofloxacin as prophylaxis against spontaneous bacterial peritonitis

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17
Q

Liver transplant criteria

A

King’s college hospital criteria
Paracettamol: pH <7.3 24h after ingestion, or INR >6.5 or creatinine raised, or grade 3-4 hep enceph
Non-paracetamol: INR>6.5 or 3 of: drug induced, <11 or >40yo, 1w between onset of jaundice and enceph, INR >3.5 or bilirubin very high

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18
Q

3 managements of alcohol withdrawal

A

Benzo for seizures
Disulfiram - makes very ill if drink as inhibition of acetaldehyde dehydrogenase
Acamprosate - reduces cravings as weak antagonist of NMDA receptors

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19
Q

Causes of budd-chiari and sx

A

Hepatic vein thrombosis, usually from procoagulable state - COCP, pregnancy, thrombophilia, polycythaemia rubra vera
= abdo pain (sudden onset and severe), ascites and tender hepatomegaly

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20
Q

Hereditary haemochromatosis - what is it and features and treatment

A

Abn iron metabolism, so increased iron abs and deposition in organs: MEALS
Myocardium - arrhythmias, dilated cardiomyopathy
Endocrine - diabetes, hypogonadism = amenorrhoea and infertility
Arthritis
Liver - chronic liver diseae = hepatocellular carcinoma
Skin - slate grey discolouration
Treat with venesection, low iron diet, transplant in cirrhosis

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21
Q

What is a1at deficiency and treatment

A

a1at inhibits neutrophil elastase in inflammatory cascade
Hepatitis in newborns, cirrhosis in adulthood, emphysema.
Manage pulmonary and hepatic complications, quit smoking, consider a1at from pooled donors

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22
Q

What is wilson’s Disease and presentation

A 
Aut rec disorder
Excess copper deposition in tissues, from increased abs from SI and decreased excretion from liver
Children - liver diseae
Adults - neuro disaee
Presents 10-25yo
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23
Q

Sx of wilson’s disease

A

Liver - hepatitis, cirrhosis
Neuro - basal ganglia degeneration (asterexis, chorea), speech and behavioural problems, dementia
Cosmetic - blue nails, Keyser fleicher rings in eyes
Renal tubular acidosis, haemolysis

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24
Q

Diagnosis of wilson’s Disease and treatment

A

Caeruloplasmin and serum copper low (copper carried by caeuroloplasmin)
Urine copper 24h excretion high
Treat with copper chelalator penicillamine

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25
Q

What is AI hepatitis

A

Suppressor T cell defects
Autoantibodies against hepatocyte surface antigens
Young/middle aged women
Present with acute hep and signs of other AI disease - fever, malaise, urticaria, polyarthritis, pulmonary infiltration, glomerulonephritis. Secondary amenorrhoea

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26
Q

AI hepatitis bloods

A

All LFTs high - gamma GT, ALP, ALT, AST
Positive autoantibodies
Anaemia, low WCC, low platelets - hyperplenism

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27
Q

Manage AI hepatitis

A

Immunosuppressants, prednisolone

Transplant if decompesated cirrhosis, or failure to respond to medication

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28
Q

Associated conditions with AI hepatitis

A 
UC
PSC
Glomerulonephritis
AI thyroiditis
AI haemolysis
Pernicious anaemia
DM
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29
Q

Viral hepatitis presentation

A

Prodrome (hep a and b) - flu-like, malaise, arthralgia, nausea
Icteral (esp hep a then b) = acute hepatitis - hepatomegaly, abdo pain, cholestasis; extrahepatic - urticaria, arthritis
Chronic (esp hep c then b) = cirrhosis, increased hepcell carcinoma risk

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30
Q

Hep b serology

A 
HBsAg = acute disease.  Present for >6m = chronic inf
Anti-HBs = immunity - exposure or immunisation. Neg in chronic disease
Anti-HBc = previous (or current) infection, IgM present for about 6m, IgG Anti-HBc persists
HbeAg = breakdown of core antigen from liver cells, so indicates infectivity
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31
Q

Diabetes complications and glucose levels for diagnosis

A

CVS disease, renal disease - can give kidney and pancreas transplant if renal failure in T1DM
Retinopathy if >6.5% HbA1c
Fasting glucose >7 or >11.1 2h after 75g glucose
HbA1c 6.5% or 48mmol - 42-47 (6-6.4%) = prediabetic

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32
Q

Insulin.’s role and cause of diabetes

A 
Fuels metabolism and glucose uptake
Inhibits protein catabolism 
Fatty acid clearance
Active transport of aa into cells
Inhibits gluconeongenesis and liver glycogen breakdown

Diabetes = abnormality in molecule, receptor or signalling

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33
Q

Sx of diabetes

A 
Urinating
Thirsty
Hungry
Blurred vision
Fatigue 
Slow healing
Weight loss - T1
Tinging or numbness in hands/feet - T2
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34
Q

Type 1 dm pathophysiology

A

AI destruction of B cells at varying rates = absolute insulin deficiency
Insulin suppresses ketone production, so no insulin = ketones = emergency
Autoantibodies and HLA associations

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35
Q

T1 dm management incl 1st regime in newly diagnosed adults and sick day rules

A

Patient education (for exercise, illness, food), home glucose monitoring, DAFNE course, HbA1c regularly
Start basal-bolus with 2x/d insulin detemir = long acting and soluble/rapid acting insulin for meals and correct high BMs
Sick day rule - never stop basal insulin
- continue meal time insulin and add extra:
— minor = +- ketones in urine, increase total in day and take correction
— major = ++ ketones in urine, increase background by a lot and take correction. Get help if ketones don’t fall in 2-4h

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36
Q

Indications for insulin sc pump and use

A

HbA1c stays >8.5%
Regular hypos from trying to control HbA1c
Can adjust basal rate throughout day

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37
Q

DM2 cause

A

Insulin resistance (levels may be high)
- pancreas creates more - eventually exhaustion - hyperglycaemia
Obesity

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38
Q

Insulin after bariatric surgery - 4

A

Fasting blood glucose normalises within 7d
Liver fat content falls
Insulin sensitivity normalises, then insulin release goes back to normal in 8w
Decrease in pancreatic fat = B cell function normalises

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39
Q

DM2 management categories

A

Diet and exercise
Anti obesity drugs
Hypoglycaemics - metformin, sulphonylurea, thiazolinodione, GLP-1 receptor analogue, DPP4 inhibitor
Insulin

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40
Q

What does metformin do and ADRs

A

Metformin = decreases gluconeogenesis and action of glucagon. Increases glucagon uptake peripherally
ADR - GI, rare = lactic acidosis
Don’t give if liver/renal failure

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41
Q

What does sulphonylurea do and ADR

A

Gliclazide - stimulates release of endogenous insulin. Decrease microvascular risk
ADR - hypoglycaemia, weight gain

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42
Q

What does thiazolinodione do and ADR

A

Pioglitazone - increase PPAR-Y, stimulating transcription of GLUT-1 and 4 - insulin sensitiser = increase glucose uptake
ADR - oedema and weight gain. Not if HF or osteoporosis/bone fracture risk

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43
Q

What does GLP-1 receptor analogue do and associated drug

A

Exenatide - increase response to glucose in GI, so stimulating insulin annd suppressing glucagon secretion = glucose-dependent
Weight loss, slows gastric emptying, increases satiety
ADR - GI = nvd, headache and dizzy

DPP4 inhibitor sitagliptin prevents incretin hormones GLP1 and GIP breakdown

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44
Q

DM medication in surgery

A

Variable rate insulin infusion if will miss more than 1 consecutive meal or emergency surgery
Don’t take med in morning if NBM, except metformin and pioglitazone

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45
Q

Insulin storage and where to use

A

In fridge until opened, then room temp. Use within 30d of opening
Don’t use other people’s insulin
SC pen into abdo or outer thigh, hold pen in for 10s
Also pump or syringes

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46
Q

Different types of insulin

A

Rapid = novorapid, 15m onset, 30-60m peak, 4h duration
Short acting = actrapid, 30m - 2h - 6-8h
Intermediate = humulin I, 2h - 4-6h - 14h
Long = lantus, 2h - no peak - 24h duration
Glargine - high strength, once a day, flatter and prolonged conc

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47
Q

When to use insulin infusion, adv and disadvantages and risks

A

DKA, HONK/HOHG
Surgery, major vascular event (CVA)
Vomiting, metabolically unwell (sepsis)
Enterally fed
Adv - control with target to improve clinical outcomes, avoid metabolic decompensation
Disadvantages - invasive, requires regular BM monitoring, difficult to control if patient is eating, prolongs stay
Risks - rebound hyperglycaemia or DKA if stopped suddenly; hyper-o-glycaemia if inadequate rate or monitoring; fluid overload; hypokalaemia/natraemia; line infection

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48
Q

Practicality of setting up insulin infusion and stopping

A

50 units of actrapid, mix with 49.5ml saline in 50ml insulin syringe, set up IV insulin syringe driver
Review unstable BMs, assess rate/12h and need for infusion and fluids /24h
Continue until eating and drinking and back on usual DM drugs for 30m, then BM every 4h for 24h for no rebound hyperglycaemia

Measure BM every 1h for 12h then change rate if no effect
Can be reduced if sensitive, intermediate or increased rate if insulin resistance

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49
Q

Manage hypoglycaemia

A

<4mmol - 75ml of 20% dextrose over 15m, repeat if still <4
ACS or stroke - keep above 6mmol
Renal/cardiac disease - may need 10% dextrose
Once >4mmol, restart infusion

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50
Q

5 types of diabetes - not T1 or T2

A
  1. MODY - Maturity Onset Diabetes of the Young - B cell defect, aut dom, defect in insulin action at receptor
  2. Gestational diabetes - normally 3rd trimester
  3. Pancreatic (exocrine) related diabetes - pancreatitis, trauma, pancreatectomy, carcinoma
  4. Drug-related diabetes - thiazides, b blockers, psychotropics, glucocorticoids
  5. Growth hormone causes insulin resistance - acromegaly, Cushing’s
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51
Q

Complications of dm - acute and chronic

A

Acute - DKA, HONK
Chronic - microvascular (retinopathy, neuropathy, nephropathy)
- macrovascular (cerebrovascular, peripheral vascular, cardiovascular)

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52
Q

DKA cause, presentation, diagnosis

A

Non-compliance, or increased insulin requirements for stress - infection, MI
1. BM >11mmol or known DM
2. Ketones >3mmol/l blood or >2+ urine
3. Venous pH <7.3 +- bicarbonate <15mmol/l
= abdo pain, vomit, drowsy, dehydration, ketotic breath, hyperventilation

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53
Q

DKA management incl inv

A 
VBG - pH, ketones, glucose, bicarb
U&amp;E - Na, K
FBC and cultures
ECG, CXR, MSU
Continuous cardiac and pulse ox monitoring

50u actrapid in 50ml NaCl 0.9%, infusion at 0.1u/kg/h
Continue long acting insulin

Check pH, bicarb, K and glucose at 1h, 2h and every 2h, for:
- ketones <0.5mmol/l/h OR
- bicarb up by 3mmol/l/h and glucose down by 3mmol/l/h
Increase by 1u/h until reaching targets

Consider catheter, aim for 0.5ml/kg/h
Start LMWH
When glucose <14mmol, start 10% dextrose at 125ml/h alongside saline

Continue fixed rate until:
- ketones <0.3mmol/l
- pH >7.3
- bicarb >18mmol/l
Urinary ketones will stay positive until after resolution

Find and treat inf/cause

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54
Q

Complications of dka - 5

A

Cerebral oedema from fluid overload
Hypophosphataemia, hypokalaemia
Thromboembolism
Aspiration pneumonia

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55
Q

What is HONK and treatment

A

Generally elderly DM2

  1. Hyperglycaemia >30mmol/l
  2. Hyperosmolar
  3. Hypovolaemia - don’t appear dehydrated as preserved intravascular volume
  4. Ketones <3 and HCO3 >15, pH >7.3

Osmotic diuresis due to increased glucose - water losses greater than Na and K
Long standing - 1w plus - extreme dehydration and metabolic disturbances

Treatment aims to reduce osmolality, replace fluids and electrolytes and normalise blood glucose
Treat underlying cause and prevent VTE
Insulin needed if any ketonaemia

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56
Q

Diag of hypoglycaemia and causes

A

Whipple’s triad: BM<3, symptoms, relief of symptoms with glucose admin

Hypoglycaemia and unwell:

  • drug induced - insulin or alcohol
  • hormone def - Addison’s
  • organ failure - liver, chronic renal failure
  • tumour - non-Islet cell tumour

Hypoglycaemia and well:

  • insulinoma
  • non-islet cell tumour - adrenal carcinoma, hepatocellular carcinoma, lymphoma
  • functional B cell disorder
  • AI
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57
Q

Sx of hypoglycaemia and treatment

A

Autonomic/adrenergic when BM2.5-3: sweating, hunger, tingling, trembling, palpitations, anxiety
Neuroglycopoenic when BM<2.5: visual disturbance, personality change, confusion poor concentration, lethargy, coma when <2

Eat carbs, glucogel, 100mll 20% dextrose, IM/SC 1ml glucagon

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58
Q

DM in pregnancy - before and during, and risks

A 
Optimise HbA1c - not recommended to get pregnant if >86
Lose weight, smoking, alcohol, high dose folic acid, assess other teratogens eg ACEi
Screen for retinopathy and nephropathy
Increased risk of:
- hypo during first trimester esp
- worsening retinopathy and nephropathy - check every trimester
- pre eclampsia
- thromboembolic disease
- DKA (+ potential foetal loss)
Foetal risks:
- cardiac, neural tube and renal defects
- preterm
- macrosomia
- foetal mortality and still birth
- NNU
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59
Q

Paeds DM

A

Random blood glucose >11.1 = diabetic - inpatient for 3d and teach amount insulin, diet etc

Start on 0.5u/kg/d. Basal in morning if <5yo, evening when >5yo, then 2 doses when puberty. Increase to 2u/kg/d in puberty as hormones = insulin resistance

Stabilise around 20yo

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60
Q

Elderly DM

A

More likely to have hypos due to 5+ drugs, poor diet, chronic kidney problems, more susceptible to illnesses
Exercise and diet harder
Cognitive complicatiotns more likely

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61
Q

Pathogenesis of diabetic eye disease and stages

A

10y after onset, damage to small blood vessels, also cataracts more common
Microvascular disease - retinal ischaemia - increased VEGF - new vessel formation
1. Background retinopathy = dots (micro aneurysms) and blots (haemorrhages) and hard exudates (yellow lipid patches)
2. Pre-proliferative retinopathy = cotton wool spots (retinal infarcts), multiple blot haemorrhages, venous bleeding and microvascular abnormalities
3. Proliferative = new vessels on disc and elsewhere, fibrovascular proliferation and tractional retinal detachment. Pre-retinal or vitreous haemorrhage
4. Maculopathy - exudate within 1 disc diameter of centre of fovea, group of exudates in macula, retinal thickening

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62
Q

Inv diabetic eye disease and treatment

A

Fluorescein angiography, eye screening

Trt

  • control: glycaemia, blood pressure, lipids
  • antiplatelet therapy
  • lifestyle - smoking, alcohol, exercise
  • laser treatment, VEGF inhibitors
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63
Q

RF for worse diabetic retinopathy

A

Smoking in DM1, glucose control, systemic htn, blood lipids

Age, race, genetic predisposition, pregnancy, duration of diabetes

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64
Q

Renal disease in DM

A

Leading cause of end stage renal disease
Proteinuria + DM
Main RF is time with diabetes
Likely to also have renal impairment, retinopathy and hypertension

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65
Q

Neuropathy in DM

A

Distal axonal loss from focal demyelination = reduced nerve conduction velocity or loss of nerve function
Causes: neuropathic ulcers, erectile dysfunction (autonomic neuropathy), altered sensation (pain and incresed sensitivity), Charcot arthropathy

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66
Q

What is Charcot foot

A

Sympathetic nerve loss = increased blood flow to foot
= increased osteoclast activity and bone turnover,
so foot more susceptible to damage,
and any trauma = destructive changes

Mostly tarsal-metatarsal or metatarso-phalangeal joints.
Warm, swollen and painful foot
X-ray = osteolytic changes, fractures and joint reorganisation
Subluxation of metotarsophalangeal and dislocation of large joints
Identify early and immobile to prevent joint destruction

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67
Q

Macrovascular risk in DM and factors to control

A

2-4x increased risk of MI
Peripheral vascular disease in 10%
75% will die of macrovascular disease
Prevent with BM, lipid and bp control, smoking and weight loss
First line = always ACEi and target 140/80

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68
Q

Hypertension in DM

A

Insulin resistance, hyperinsulinanemia

Assoc with earlier microalbuminuria and nephropathy

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69
Q

What is lipid disease and who gets it

A

Combination of genetic and envirnemental factors. Primary = normally genetic, Secondary = obesity and DM2 are biggest factors. RF:

  • premature CHD
  • atherosclerosis
  • diabetes or insulin resistance
  • post-menopausal females not on HRT
  • alcohol
  • family hx of hyperlipidaemia, early CHD or atherosclerotic disease
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70
Q

Manage lipid disease

A

Lower cholesterol - 10% loss = 25% reduction in CVS risk

Statin - HMG-CoA reductase inhibitor decreases rate limiting step in cholesterol synthesis in liver = increases LDL receptors to increase clearance.

  • CYP3A4 metabolism, avoid grapefruit juice, can interact with ciclosporin
  • 1st line if LDL or mixed high

Fibrate - better for increasing HDL and reducing triglycerides by increasing lipoprotein lipase activity and LDL receptor mediated LDL clearance

  • ADR nausea, anorexia, diarrhoea, gallstones, myopathy (esp with statin)
  • 1st line if LDL high, 2nd line with statin if TAG or mixed

Bile acid sequestration - safe in pregnancy, ADR = GI sx

Cholesterol absorpation blocker ezetimibe - with or instead of statin, inhibits dietary and biliary LDL absorption
- use 2nd line to statins if LDL only high

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71
Q

Where is the pituitary and what does it release

A

Sella turca in base of brain
[FLAGToPa]
Ant pit - FSH, LH, ACTH, GH, TSH, PTH
Post pit - oxytocin, ADH

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72
Q

Disorders of the hypothalamus - causes and effect

A

Decreased production of all hormones except prolactin as hypothalamus suppresses this
- from trauma/surgery, radiotherapy, SIADH (excess)

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73
Q

Hyperpituitarism and treatment

A

Prolactinoma adenoma - excess prolactin production, reduced production of other hormones
- more in women - oligo, amenorrhoea, infertility (interfere with GnRH)
- Galactorrhoea, erectile dysfunction, visua field defects and headache
Suppression test, treat with dopamine agonist bromocriptine

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74
Q

Hypopituitarism cause and sx

A

Non-functioning adenoma, suppresses pituitary functions by compression in order of GH, LH, FSH, ACTH, TSH, prolactin
Sx - depression, tiredness, hypogonadism
- headache, vomiting, papilloedema
- visual disturbance, CN palsy
- oligo/amenorrhoea, reduced libido, infertility in men
Surrounding tumours - craniopharyngioma, glioma, meninioma, mets (bronchus, breast)
Pit infarction from sheehan’s = panhypopituitiarism - no lactate, amenorrhoea, death

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75
Q

Inv hypopituitarism and treat

A

Basal hormone level and stimulating hormone
Inhibition eg synACTHen
Visual field test
MRI, CT

Treat with all hormone replacement except prolactin

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76
Q

Post pituitary diseases - 2

A

Diabetes insipidus - defective ADH production = plasma osmolality very high, urine osmolality low, clinical features.
- Can cause fatal dehydration
SIADH - from inf, neuro, endocrine, malignancy diseases = plasma osmolality very low, hyponatraemia, urine osmolality very high with high sodium in urine
- malaise, weakness, confusion, coma

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77
Q

What are T3 and T4 bound to in blood

A

Albumin

TBG, TTR

78
Q

Hyperthyroidism symptoms, exam and treatment

A

Sx - sweating, palpitations, irritability, overheating, hyperactivity, insomnia, pruritis, increased stool frequency, thirst and polyuria, oligomenorrhoea
Exam - sinus tachycardia, AF, palmar erythema, fine tremor, hyperkinesia, hyperreflexia, wam and moist, hair loss, muscle wasting

Grave’s - diffuse goitre, exophthalmos, optic neuropathy, periorbital oedema, gritty eye, retrobulbar pressure pain - from grave’s antibodies

Treat

  • carbimazole for 1y, usually only works once, then monitor once off treatment. ADR = GI upset, agranulocytosis
  • surgery - risk of RLN damage
  • radioiodine
79
Q

ADR of thyroidectomy

A 
Local haemorrhage causing laryngeal oedema
Wound infection 
Thyroid storm
Hypoparathyroid
RLN damage
80
Q

What happen when someone with hyperthyroid gets infection

A

Thyroid storm:
Altered mental status, tachycardia, fever, vomiting, diarrhoea and jaundice
Treat in ITU and monitor cardiac, fluid and cooling
- digoxin for arrhythmia once hypokalaemia corrected

81
Q

Secondary hyperthyroid?

A

From TSH secreting adenoma or reistance to thyroid hormone

82
Q

Hypothyroid cause and sx

A

Inflammation in thyroid, normally from Hashimoto’s. Causes transient hyperthyroid then hypothyroid. Thyroid is lymphocitic and fibrotic - painless, variably sized goitre
Sx - fatigue, lethargy, constipation, menorrhagia then oligo/amenorrhoea, cold intolerance, muscle stiffness, cramps, dry skin and hair loss, deep hoarse voice, OSA, decreased visual acuity
Treat with levothryoxine, increasing dose slowly. May need increase 25-50% during pregnancy, abs reduced in coeliac or atrophic gastritis

83
Q

Hypothyroidism and infection?

A

Myxoedema coma
Treat in ICU with external warming (0.5degree/h). Monitor for arrhythmia, hypoglycaemia, hyponatraemia. Treat illness - abx

84
Q

Thyroid cancer

A

Biggest risk is radiation <20yo
Solitary nodule or increasing goitre size

80% papillary thyroid carcinoma - 20-30yo, treat with surgery, adjuvant radioiodine

Follicular thyroid carcinoma - 50yo, mets haematogenous spread to lung and bones

Lifelong follow up as can recurr

85
Q

What is sick euthyroid

A

TSH in normal range, T3 and 4 low

86
Q

Causes of primary hyperaldosteronism - 3

A

Biateral adrenal hyperplasia
Conn’s syndrome
Adrenal carcinoma

87
Q

Main features of bilateral adrenal hyperplasia and treatment

A

Aldosterone = inhibit renin secretion, increase sodium reabsorption and potassium and hydrogen secretion = hypokalaemia alkalosis
- most common cause of secondary hypertension (10% of htn)
- resistant to conventional treatment
- LV hypertrophy
Treat with mineralocorticoid receptor antagonist spironolactone if not fit for surgery
Surgery - laparoscopic adrenalectomy

88
Q

Sx of Cushing’s syndrome and diagnosis of cause

A

Excess cortisol - ACTH dependent (from pituitary adenoma = Cushing’s disease, suppressed with high dose dexamethasone, or ectopic tumour) or ACTH independent (adrenal tumour)

Round face, skin thin, striae on breasts, abdo and thigh, acne and hirsuitism
Weight gain - buffalo hump, truncal obesity, prox muscle weakness
Mood disturbance, insomnia, depression, psychosis
Menstrual disturbance, low libido
High VTE risk

Hypokalaemia metabolic alkalosis

89
Q

Assoc features with Cushing’s syndrome

A 
Hypertension
Impaired glucose tolerance, DM2
Osteopoenia/osteoporosis
Vascular disease from metabolic syndrome
Infection susceptibility
90
Q

Treat cushing’s

A

Transphenoidal surgery if Cushing’s disease, or pituitary radiotherapy
Adrenalectomy

91
Q

Adrenal insufficiency causes and inv

A

Lack of mineralocorticoids and glucocorticoids
Primary - mostly AI (addison’s), or TB
- no response to synACTHen test
Secondary - hypopituitarism or hypothalamus disorder
- responds to synACTHen, no pigmentation as no ACTH
Adrenal incidentaloma - found on imaging for something else, determine if functional +- malignant
Follow up for 3y then discharge if benign and non functioning
Remove if >4cm, malignant or functioning

92
Q

Addison’s sx

A

Depression and lethargy
Weight loss, abdo pain, anorexia, nvd/constipation
Hypoglycaemia
Postural hypotension
Pigmentation from lack of cortisol neg feedback ACTH and POMC secretion = stimulates melatonin receptor
Vitiligo
Addisonian crisis

93
Q

Treat addisons

A

Hydrocortisone and fludrocortisone, wear med alert bracelet and steroid card, increase if ill
Wean off slowly

94
Q

Addisonian crisis sx, cause and treat

A

Increased heart rate, postural drop
Oliguria, confusion, hypoglycaemia
From trauma, inf, surgery and stopping long term steroids
Hydrocortisone IV, crystalloid (glucose)

95
Q

Causes of hypercalcaemia

A

Main are malignancy (bone mets, myeloma) or primary hyperparathyroidism
Less common = Addison’s, Sarcoidosis
Drugs - lithium, thiazides
Renal failure

96
Q

Sx of hypercalcaemia

A 
Stones, polyuria, polydipsia
Anorexia, constipation, abdo pain, vomiting
Confusion, lethargy, depression 
Pruritis, sore eyes
Eventually - renal failure, hypertension
97
Q

Primary hyperparathyroidism and sx and presentations

A

From parathyroid adenoma or hyperplasia
Asymptomatic or features of hypercalcaemia
Stones - renal stones, polyuria
Moans - depression
Bones - osteopororis, pathological fractures
Groans - abdo pain, nv, constipation, pancreatitis

98
Q

Inv hyperparathyroidism

A

Calcium high
PTH normal or high
ALP high
Phosphate low

99
Q

Treat hyperparathyroidism and complications

A

Remove
Observe if mild
Complications of surgery - vocal cord paresis from RLN palsy, tracheal compression from haematoma, hypocalcaemia

100
Q

Inv and treat hypercalcaemia of malignancy

A

High calcium, low PTH

Aggressive rehydration and zolidronic acid

101
Q

Causes of hypocalcaemia and sx

A

With high phosphate: from hypoparathyroid dysfunction - infiltration, radiation, surgery. Or CKD
With normal or low phosophate: impaired bone release - osteomalacia. Or acute pancreatitis or DiGeorge syndrome

Sx from increased muscle excitability = SPASMODIC:
Spasms - carbopedal (Troussea’s sign)
Periorbital paraesthesia
Anxious, irritable, irrational
Seizures
Muscle tone increased in smooth muscle - wheeze, colic, dysphagia
Orientation impaired - confusion
Dermatitis
Impetigo herpetiformis (very serious in pregnancy if low Ca and pustules)
Chvostek’s sign: 3Cs: choreoathetosis, cataracts, cardiomyopathy (long qt)

102
Q

Inv and treat hypocalcaemia

A

Inv - low calcium, high, low or normal phosphate, high PTH, normal ALP
Treat - calcium supplements, calcitriol
Calcium gluconate if acute tetany and seizures

103
Q

Vit d deficiency causes and treatment

A

Sunlight, diet, secondary hypoparathyroid - malabsorpation gastrectomy
Calciferol, correct biochem abn, heal bone abn

104
Q

What is pseudohypoparathyroid, inv and treat

A

Target organs don’t respond to PTH
Short stature, short 4th and 5th metacarpals
Inv - low calcium, high PTH
Give calcium and calcitriol

105
Q

What is premature ovarian insufficiency

A

3: 1. Amenorrhoea, 2. oestrogen def and 3. elevated gonadotrophins
<40yo
Due to ovarian follicular failure and accelerated depletion of ovarian germ cells
Sx - amenorrhoea, sx of oestrogen def, other AI conditions, FSH >40 x2 and low oestradiol levels

106
Q

What is Turner’s syndrome and management

A

45XO
Short, wide spaced nipples, webbed neck
Gonadal dysgenesis, amenorrhoea, no SSC
Aortic dissection, coeliac disease, congenital renal abnormalities
Give sex hormone replacement and managecomlicatiotns

107
Q

HRT advantages and disadvantages

A

Adv
- reduce risks of CVD and osteoporosis
- reduce flushes, vaginal atrophy, urinary sx
Disadv
- breast tenderness, mood changes, irregular bleeding
- risk of breast cancer, endometrial cancer, gall stones, migraines, endometriosis and uterine fibroids, liver disease

108
Q

What is primary hypogonadism and sx

A

Testicular failure with normal hypothalamus and pituitary
Before puberty: penis <5cm, testes volume <5ml, no rugae or pigmentation, gynaecomastia, high voice, central fat distribution, delayed bone age
After puberty: osteoporosis, central fat distribution, gynaecomastia, anaemia

109
Q

What is secondary hypogonadism

A

By hypothalamic/pituitary dysfunction eg Kallman’s - failure of GnRH producing neurones to migrate to hypothalamus - and anosmia

110
Q

What is Klinefelter’s - sx, inv and treatment

A

47XXY
Small testes, gynaecomastia, tall, features of hypogonad, cognitive dysfunction
Less facial hair, reduced libido and ED, infertility, obesity

Low T, raised LH and FSH

Risk DM2, VTE, osteoporosis, malignancies

Treat - lifelong androgen replacements

111
Q

Androgen replacement therapy

A

For libido, mood, muscle mass, sexual function
Prevent osteoporosis
Will need gonadotrophins to initiate and stimulate spermatogenesis if want fertility

Risks - prostate cancer, acne CVS disease, polycythaemia, gynaecomastia, fluid retention, hepatotoxicity, OSA

112
Q

What is obesity and its staging and consequences

A

Excess of body fat sufficient to adversely affect health
0 - no risk factors, no physical sx or functional limitations
1 - sx of physical limitation (exertional SOB) and subclinical conditions (borderline htn, impaired fasting glucose, elevated liver enz)
2 - chronic conditions - DM2, htn, OSA, GORD, PCOS
3 - end organ damage - MI, HF, DM complications, significant impairment to wellbeing
4 - disabilities from obesity related chronic disease
Consequences - dyslipidaemia, stroke, asthma, htn, DM2

113
Q

Treat obesity

A

Orlistat - pancreatic lipase inhibitor, reducing fat absorption from GI
Bariatric surgery - gastric bypass, sleeve gastrectomy, adjustable gastric banding

114
Q

What is carcinoid syndrome and sx

A

10% part of MEN
Neuroendocrine tumours of enterochromaffin cell which produces 5HT

Sx: FIVE-HT; presents with GI signs
Flushing, Intestinal (abdo pain, appendicitis, intussusception, obstuction, diarrhoea), Valve fibrosis (pulmonary stenosis, tricuspid regurg), whEEze, Hepatic involvement (bypassed first metabolism), Tryptophan def

Crisis = tumour outgrows blood supply or handled too much = mediator release
- vasodilation, hypotension, bronchoconstriction, hyperglycaemia

115
Q

What is MEN

A 
Multiple Endocrine Neoplasia:
PAP, FPP, FPMM
1 - aut dom, aggressive, high mortality, 2/3 of:
Parathyroid tumour/hyperplasia; 
Ant pit adenoma; 
Pancreatic neuroendocrine tumour 
2a - 
Familial medullary thyroid carcinoma
Phaechromocytoma
Parathyroid 
2b - 
Familial medullary thyroid carcinoma
Phaechromocytoma
Mucosal neuromas
Marfanoid habittus
116
Q

Acromegaly causes

A

Pituitary tumour - 99%
Ectopic GH releasing tumour
Assoc with Men1

117
Q

Sx of acromegaly

A

Acroparaesthesia, arthralgia, back ache
Amenorrhoea, redued libido
Headache, sweating, snoring
Signs - hands, supra orbital ridge, wide nose, coarse facial features, macroglossia
Acanthosis nigricans
OSA, carpal tunnnel
Pit mass effect - hypopituitarism, vision, hemianopia, fits

118
Q

Complications of acromegaly

A

CCF or ketoacidosis
Impaired glucose tolerance
Vascular - raised BP, LV hypertrophy, cardiomyopathy, arrhythmia, IHD, stroke
Colon cancer risk

119
Q

Tests for acromegaly

A

Increased glucose, phosphate and calcium
Don’t trust GH test as pulsatile - increase in sleep and stress
If high, or IGF1 high = OGTT
- GH normally suppressed by glucose so hardly detectable in normal person - not suppressed in acromegaly
MRI pituitary fossa
Hypopituitarism inv and visual fields and acuity
ECG and echo

120
Q

Treat acromegaly

A

Transphenoidal surgery
If that doesn’t reduce GH and IGF1 = somatostatin analogue
If doesn’t work = GH antagonist

121
Q

Phaeochromocytoma what is it

A

Tumour of sympathetic paraganglia cells in adrenal cortex, secretes catecholamines
Can be bilateral, extra-adrenal, linked to Men2
Classic triad: episodic headache, sweating, tachycardia

122
Q

Sx of phaeochromocytoma

A

Psych - anxiety, panic, hyperactive, psychosis
CNS - visual disturbance, headache, dizzy, fits, Horner’s
Heart - arrhythmia, VT, angina, MI, SOB, faint, cardiomyopathy
GI - dv, abdo pain over site, mass
Others - sweating, heat intolerance, temp, haemoptysis, pallor

123
Q

Tests for phaeochromocytoma

A

WCC raised
Urine metadrenaline 3 x 24h and plasma
Clonidine suppression test

124
Q

Treat phaeochromocytoma

A

A and b blockade pre-op - a first to avoid unopposed a-adrenergic stimulation

125
Q

Key substances controlled by kidney

A

Na, K, Ca, PO4
Epo, renin
25,hydroxyvitD to 125,dihydroxyvitD

126
Q

RAAS mechanism

A

From JGA in response to reduced flow or sympathetic stimulation
- convert angiotensinogen to angiotensin 1, which is then converted to angiotensin 2 by ACE. Angiotensin 2:
— constricts efferent arteriol and peripheral vasoconstriction
— stimulates adrenal cortex to release aldosterone which activates NaK pump - for Na and H20 absorpation with K and H loss

127
Q

Cause, sx and treatment of hypernatraemia

A

Due to water loss in excess of sodium: diabetes insipidus, hyperaldosteronism, fluid loss, osmotic diuresis, incorrect fluid replacement
Sx - weakness, lethargy, irritability, thirst, coma and fits
Give water, or 5% dextrose, or saline if hypovolaemia

128
Q

Sx and treatment of hyponatraemia

A

Sx - nausea and anorexia, malaise, headache, irritability, confusion, weakness, seizures
Asymptomatic chronic hyponatraemia - fluid restriction, +- ADH antagonist demeclocycline
Acute/symptomatic hyponatraemia - cautious rehydration with saline, - slowly to avoid fatal pontine demyelination - furosemide if not hypovolaemic to avoid fluid overloaded

129
Q

Cause of hyponatraemia and oedema

A

Nephrotic syndrome
Cardiac failure
Liver cirrhosis
Renal failure

130
Q

Hyponatraemia with normal urine osmolality

A

Water overload

Glucocorticoid insufficiency

131
Q

Hyponatraemia with increase urine osmolality

A

SIADH

132
Q

Hyponatraemia, dehydration and high urine sodium

A

Addison’s
Renal failure
Diuretics
Osmolar diuresis

133
Q

Hyponatraemia, dehydration and low urine sodium

A 
Water and sodium loss other than kidneys:
Diarrhoea, vomiting, burns
Small bowel obstruction, CF
Trauma
Heat exposure
134
Q

Hyperkalaemia level, cause, sx and treatment

A

> 6.5mmol/l = emergency
From: K sparing diuretics, metabolic acidosis, rhabdomyolysis, oliguric renal failure, ACEi, Addison’s
Sx: fast irregular pulse, palpitations, chest pain, weakness, lightheaded
ECG: tall tented T, wide qrs, small p, VF
Treat: calcium resonium binds K in GI, preventing reabsorption, over a few days
Emergency: calcium gluconate to stabilise heart membrane) 10ml 10% calcium gluconate) and 10u actrapid in 50ml 20% glucose to drive K into cells

135
Q

Causes of hypokalaemia and main drug effect

A

Diuretics
Vomiting and diarrhoea
Cushing’s, Conn’s
Renal tubular failure, alkalosis

Exacerbates digoxin toxicity

136
Q

Signs of hypokalaemia

A

Muscle weakness,hypotonia, hyporeflexia
Cramps, tetany
Palpiations, light headed

137
Q

Treat hypokalaemia

A

Oral K if mild
IV K cautiously, no more than 20mmol/h, if severe <2.5 - never stat bolus
Continuous ecg

138
Q

Symptoms of acidosis

A 
Kussmaul breathing 
Decreased myocardial contractility, arteriodilatation, venoconstriction
Resistant arrhythmias (VF)
139
Q

Anion gap formula

A

(Na + K) - (Cl + HCO3)

140
Q

Causes of increased anion gap acidosis

A 
KUSMAL
Ketones
Uraemia
Salicylate
Methanol
Aldehydes
Lactic acidosis
141
Q

Treat acidosis

A

Sodium bicarb if pH <7 and impaired cardiac performance

Don’t give bicarb in DKA as delays removal of ketone bodies

142
Q

Causes of metaoblic alkalosis including drugs

A

Vomiting, burns
Diuretics
CF
Laxatives, bicarb, penicillins, massive transfusion

143
Q

Sx of metabolic alkalosis

A

Most sx from hypovolaemia or hypokalaemia
From decreased cerebral and cardiac perfusion - headache, confusion, seizures, angina, arrhythmias
Compensatory hypoventilation or hypocapnoea

144
Q

Manage metabolic alkalosis

A

Treat cause

- KCl if low K, stop drugs causing it

145
Q

Electrolytes in Hartmann’s

A

Na, Cl, K, HCO3, Ca, lactate

146
Q

Distribution of saline and 5% dextrose

A

Saline - same Na concentration as plasma (150mmol/l), extracellular compartment, takes time to reach intracellular
5% dextrose - liver metabolises dextrose quickly so the water rapidly equilibrates across all compartments - useless in resusc as 1/9 stays in intravascular space

147
Q

5 causes of transient haematuria

A 
Exercise
Sex
Viral illness
Trauma
Menstruation
148
Q

Glomerular causes of haematuria

A

IgA nephropathy
Alport’s
Focal GN

149
Q

Upper urinary tract causes of haematuria

A

Stones, pyelonephritis
<40yo - trauma, polycystic kidney disease, ureteral structure
>40yo - renal cell carcinoma, transitional cell tumour, renal TB

150
Q

Lower urinary tract causes of haematuuria

A

Cystitis, prostatitis, bladder cancer, prostate cancer
<40yo - urethral stricture
>40yo - BPH

151
Q

RF for malignancy with haematuria

A

> 40yo, gross haematuria
Pelvic irradiation, occupational exposure
Smoking, alcohol, analgesia abuse

152
Q

Signs suggestive of glomerular lesion

A

Proteinuria
Dysmorphic red cells and red cell casts
Renal impairment, high blood pressure

153
Q

Inv for macroscopic haematuria

A

Urine cytology and MC&S
Cystoscopy, CT with and without contrast
FBC, U&E, G&S, clotting, PSA, Hb

154
Q

Inv for microscopic haematuria

A 
Repeat dipstick after 1w
Urine MCS and PCR and cytology x3
eGFR
CT, USS
Nephrology workup
155
Q

Diagnostic criteria for AKI - 3

A

Urine = <0.5ml/kg/h for 6h
Serum creatinine >26.5micromol/l within 48h
Serum creatinine >1.5x baseline

156
Q

3 stages of AKI

A 
KDIGO staging:
Urine output:
1 - <0.5ml/kg/h for 6h
2 - <0.5ml/kg/h for 12h
3 - <0.3ml/kg/h for 24h or anuria for 12h
Serum creatinine rise above baseline:
1 - >1.5x
2 - 2-2.9x
3 - >3x
157
Q

3 categories of AKI and causes

A

Prerenal - hypovolaemia, sepsis (vasodilation and reduced CO)
Intrinsic renal - renal parenchyma = ATN, glomerular apparatus or interstitial damage
Postrenal - obstuction causing backflow - must have both blocked, or only 1 kidney to get AKI

158
Q

RF for AKI

A

Age
CKD, diabetes, cardiac disease (LV dysfunction), myeloma
Volume depletion
Surgery
Drugs causing renal vasomotor changes - ACEi, ARB, NSAIDs

159
Q

Presenting features of AKI

A 
Non-specifically unwell, deteriorating
Hypovolaemia, or fluid overload causing pulmonary oedema
Decreased urine output
Increasing urea and creatinine 
Hyperkalaemia
160
Q

Imaging for AKI

A

Renal USS

CXR - sepsis?

161
Q

Complications of AKI - 4

A

Pulmonary oedema
Uraemia
Acidaemia
Hyperkalaemia

162
Q

Manage AKI

A

Fluid resusc until improved signs of volume depletion:
Reduced tachycardia, rising BP, visible JVP, improved urine output
Assess volume status
Remove nephrotoxic drugs

163
Q

Indications for renal replacement therpay in AKI

A 
K >6.5
Fluid overload (pulmonary oedema) refractory to medical treatment 
Relative indications: 
Acidosis pH<7.2
Critically unwell
Hyperthermia
Toxin removal
Uraemic complications
Diuretic resistance in cardiac failure
164
Q

CKD classification

A

Ideally should be 2 readings 3 months apart
1 - GFR >90 WITH evidence of kidney damage
2 - GFR 60-89 WITH evidence of kidney damage
3a - GFR 45-59 (+- evidence of kidney damage)
3b - GFR 30-44 (+- evidence of kidney damage)
4 - GFR 15-29
5 - GFR <15 = end stage, or approaching end stage
5D - GFR <15, on dialysis

Evidence of kidney damage =

  • proteinuria, haematuria,
  • or abnormal renal imaging,
  • or genetic or histologically established disease
165
Q

Causes of CKD

A

Diabetes
Hypertension, atherosclerotic disease
Cystic, congenital disease, glomerulonephritis
Infective or obstructive

166
Q

Inv for CKD

A

FBC, U&E, ESR, glucose
Calcium low, phosphate and ALP high
PTH high if CKD stage 3+
Urine - MCS, cytology, ACR. Proteinuria = chronic kidney damage
Renal USS - small unless infiltration disease, look at anatomy
Biopsy and histology if rapidly progressive disease

167
Q

Anaemia in CKD and treatment and why

A

Increase in severity with stage of CKD, higher risk if black or diabetic
Normocytic normochromic with normal level of WCC and platelets, from reduced EPO production

Treat with human recombinant epo, or erythropoeisis stimulating agents in dialysis or early CKD - improve exercise capacity, reduce fatigue, improve QoL cognitive function and sleep quality
Iron in late stages of CKD

168
Q

Cause of falling phosphate in late stage CKD?

A

Renal osteodystrophy - altered bone morphology, in CKD 4 and 5 - check these
See fall in phosphate, calcium, vit D, and increase in PTH

169
Q

CVS risks with CKD - 4

A

Coronary disease
CCF
Stroke
Peripheral vascular disease

170
Q

CVS risk factors unique to CKD and manage

A 
Valvular calcification, myocardial fibrosis 
Volume overload
Anaemia
Vit D def, hyperparathyroidism 
Insulin resistance

Offer statin to everyone with CKD +- antiplatelet

171
Q

Factors affecting CKD progression

A

AKI, urine outflow obstruction (BPH) or structural/calculi (stones)
CVD, hypertension, diabetes
Multisystem disease with potential kidney involvement eg SLE
Smoking
Chronic use of NSAIDs, nephrotoxins

172
Q

Estimation of eGFR - 4 inputs

A

Sex, race, age, creatinine

= MDRD equation

173
Q

Manage hypertension in CKD and targets

A

Not diabetic, urine ACR <30mg/mmol - treat as normal
Urine ACR >30 - lisinopril or losartan (reduce intraglomerular pressure and proteinuria even if no htn)
- ACR <70mg/mmol, target BP 140/90
- ACR >70, target BP 130/80

174
Q

Role of proteinuria in CKD - 3

A

Marker for progression
Causes progression itself
Independent RF for CVS

175
Q

When to refer to nephrology with proteinuria

A

Very high ACR, +- haematuria

A bit high ACR + haematuria

176
Q

When to assess nephrotoxicc drugs and when to start dialysiss - 8 indications

A

EGFR <60

Dialysis:
GFR <15 and sx of advanced CKD - persistent nv, anorexia, malnutrition, volume overload
GFR <5-7 regardless of sx
Refractory hyperkalaemia, acidosis
Pulmonary oedema
Pericarditis, encephalopathy, neuropathy
177
Q

Definition of diabetic nephropathy, and bp/HbA1c target

A

Dipstick proteinuria in someone with diabetes
Aim for HbA1c <7% and bp <130/80 to prevent
If proteinuria, target bp <125/75

178
Q

Role of dialysis and what it can’t do compared to kidney

A

Remove excess salt, water and acid
Remove/regulate electrolytes - K, Ca, Mg, PO4
Remove waste products of metabolism

Can’t make epo or activate vit d

179
Q

How does haemodialysis work

A

Hydrostatic pressure of blood, through semi permeable membrane to dialysate on countercurrent through dialyser, to clear solutes by diffusion. Both on high pressure, doesn’t clear large molecules well
- 4h 3x/w

180
Q

What is haemofiltration and adv

A

No dialysate - clear solutes by convection, through transmembrane pressure across membrane. Need large volumes for adequate clearance, but clears large molecules better than haemodialysis. Greater haemodynamic stability so favoured in critical care

181
Q

Dialysis access?

A

AV fistula - connection between artery and vein, takes 6-8w to mature before using. Synthetic graft is second best - risk of infection and operation, but can use within days.
Care for AV fistula:
- preserve arm veins in pre-dialysis patients - no cannula between elbow and wrist
- don’t bleed AV fistula
- dont do tourniquet or BP on that arm

Temporary haemodialysis catheter for immediate use eg AKI - higher infection rate and catheter malfunction

182
Q

Complication of AV fistula

A

Infection of graft - normally needs surgical removal
Aneurysm/pseudoaneurysm at needle sites if not rotated
Distal ischaemia - flow through fistula compromising distal flow
Extravasation causing rapid limb swelling, haemodynamic compromise, compartment syndrome, secondary infection

183
Q

Adv of peritoneal dialysis

A

Residual renal function preserved
Can be at home - patient independence, mobility, patient engagement
No vascular access needed
Cheaper

Use peritoneum (cap endothelium, matrix and peritoneal mesothelium) as semipermeable membrane, has 3 different sized pores for large, small solutes and water. 1 bag of dialysate in, 1 drains from peritoneal space into other bag

184
Q

CI to peritoneal dialysis

A

Absolute = colostomy/ileostomy, hernia, abdo wall infection

Relative CI = gastroparesis, adhesions, morbid obesity, very big polycystic kidney

185
Q

Complication of peritoneal dialysis, its sx, consequences and risk factors and treatment

A

Peritonitis - can relapse, abx failure, acute and chronic ultrafiltration failure, malnutrition
Sx - abdo pain, nausea, vomiting, cloudy dialysate. Then fever and sepsis, ileus, peritonism
RF - DM2, catheter type and implantation technique

Treat with IV antibiotics - vancomycin and cephalosporin

186
Q

Advantages of renal transplant and measurement of outcomes

A

Patient survival, quality of life better
Physiological corrections of uraemia and anaemia better
Better sexual function and fertility
Better for health economy

Measure outcomes by 1) patient survival, 2) graft survival, 3) graft outcome

187
Q

Kidney transplant contraindications - 3

A

Uncontrolled infection
Uncontrolled malignancy
Life expectancy <5y

188
Q

Kidney transplant complications

A

Early - bleeding, wound infection, vascular thrombus/embolism, urinary leak, lymphocoele, early obstruction
Late - renal artery stenosis, ureteric stenosis, bladder dysfunction, skin cancer

189
Q

Immunosuppression for kidney transplant

A

Induction = intense, at time of transplant, then maintenance for life
Triple therapy including steroid

190
Q

Causes of mono arthritis and inv

A

Septic
Crystal arthropathy
Haemarthrosis
- aspirate, WCC, gram stain and culture, polarised light microscopy

Chronic = OA, psoriatic, meniscal tear, TB, foreign body

191
Q

Causes of oligo and polyarthritis

A

Oligo - crystal arthritis, psoriatic, relative, OA, ankylosing spondylitis
Poly
- symm - RA, OA, viruses
- asymm - reactive, psoriatic

Systemic disease - SLE

Finals (13 decks)

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