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Phase 2 Mine > Revision List Endocrine > Flashcards

Revision List Endocrine Flashcards

1
Q

Pathophysiology of Acromegaly

A

Increased GH secreted due to pituitary tumour or ectopic carcinoid tumour –> liver –> bind to receptors –> results in an IGF-1.
Stimulates skeletal and soft tissue growth –> gives rise to ‘giant like’ appearance and symptoms

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2
Q

Co-morbidities of acromegaly?

A 
Hypertension
Cardiovascular events 
Headache
Arthritis
Insulin
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3
Q

Symptoms of acromegaly

A 
Headache
Acral enlargement
Excess sweating
Visual deterioration
Increased weight
Amenorrhoea
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4
Q

Signs of acromegaly

A 
Rings too tight
Jaw prognathism
Coarser face
Darker pigmentation
Deep voice
Fatigue
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5
Q

Diagnosis of acromegaly

A

Plasma GH - variable
GTT - should suppress GH in normal
IGF-1 levels raised

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6
Q

Treatments of acromegaly

A
  1. Transphenoidal surgery
  2. Medical therapy
    a. Somatostatin analogues –> Lanreotide
    b. Dopamine agonists –> cabergoline/bromocriptine
    c. GH receptor antagonist
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7
Q

What is Addison’s disease?

A

Adrenal insufficiency - destruction of the adrenal cortex

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8
Q

Causes of hypoadrenalism?

A
  1. Autoimmune adrenalitis
  2. TB
  3. Amyloid infiltration
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9
Q

Symptoms of Addison’s disease?

A
  1. weight loss
  2. fatigue
  3. poor recovery from illness
  4. headache
  5. adrenal crisis
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10
Q

Signs of Addison’s disease?

A
  1. Hyperpigmentation
  2. Hypotension
  3. Low Na+, high K+
  4. Eosinophilia
  5. Borderline elevated TSH
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11
Q

What blood tests for Addison’s

A

Blood Tests:

  1. Hyponatraemia/Hyperkalaemia
  2. Hypoglycaemia
  3. Decreased cortisol <100nmol/l
  4. Eosinophilia
  5. Increased Ca2+
  6. Raised ACTH
  7. Synacthen test - synthetic ACTH should normally increase cortisol levels
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12
Q

Confirming diagnosis of Addison’s?

A 
Primary
1. Adrenal antibodies --> 21 hydroxylase antibodies detected
2. Imaging - CT
3. Genetic - 17OHP in congenital adrenal hyperplasia
Secondary
1. Steroids
2. Imaging
3. Genetic
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13
Q

How to treat adrenal insufficiency?

A
  1. Hydrocortisone
  2. Primary: fludrocortisone oral - replace mineralocorticoids
  3. Carry steroid card and bracelet
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14
Q

Symptoms of adrenal crisis?

A
  1. Fatigue
  2. Vascular collapse
  3. Dehydration
  4. Renal shut down
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15
Q

Signs of adrenal crisis?

A
  1. Hyponatraemia/Hyperkalaemia
  2. Hypotension/CVD collapse
  3. Fatigue
  4. Fever
  5. Hypoglycaemia
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16
Q

Management of adrenal crisis?

A
  1. Blood for cortisol/ACTH
  2. IV/IM hydrocortisone 100mg
  3. Fluid resuscitation 1L saline
  4. Hydrocortisone 50-100mg IV/IM
  5. If primary adrenal crisis: fludrocortisone 100-200micrograms - wean to normal replacement over 72 hours

Double dose of steroids on steroids

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17
Q

Causes of secondary adrenal insufficiency?

A

Hypopituitarism

  1. Pituitary macroadenoma
  2. Apoplexy
  3. Hypophysitis
  4. Metastases, infiltration, infection
  5. radiotherapy
  6. congenital
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18
Q

Craniopharyngioma presentation

A
  1. Visual field defects
  2. Hypopituitarism
  3. Raised ICP
  4. Growth failure
  5. Weight increase
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19
Q

Rathke’s cyst presentation

A
  1. Headache
  2. Amenorrhea
  3. Hypopituitarism
  4. Hydrocephalus
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20
Q

Meningioma presentation

A
  1. Visual field defects
  2. Loss of visual acuity
  3. Endocrine dysfunction
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21
Q

Electrolytes present in the ECF

A

Na+, Cl-, HCO3-

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22
Q

Common electrolytes in ICF

A

Potassium, magnesium, phosphate

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23
Q

Exogenous solutes that may affect osmolality?

A
  1. Alcohol
  2. Methanol
  3. Polythene
  4. Glycol
  5. Manitol
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24
Q

Output drivers of water?

A
  1. Excretion by kidney controlled by GFR and vasopressin

2. Uncontrolled insensible losses

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25
Q

Calculation for osmolality?

A

2Na+ + glucose + urea

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26
Q

What is cranial DI

A

Decreased vasopressin. Secreted from posterior pituitary

27
Q

Nephrogenic DI?

A

Impaired response to action of vasopressin

28
Q

Differential diagnosis of DI?

A

Hyperglycaemia
Hypercalcaemia
Hypokalemia

29
Q

Diagnosis of DI?

A
  1. Urinary volume>3L/day
  2. Check renal volume and serum calcium
  3. Plasma osmolality <300
  4. Hyponatremia
  5. Water deprivation test
30
Q

Causes of cranial DI?

A 
Acquired:
1. Idiopathic
2. Tumors - craniopharyngioma, germinoma
3. Infections - TB, encephalitis, meningitis
4. Vascular - aneurysm, infarction
5. Inflammatory - GBS, neurosarcoidosis
Primary:
1. Genetic:DIMOAD
2. Autosomal dominant
3. Developmental : septic optic dysplasia
31
Q

Causes of nephrogenic DI?

A

Acquired:
1. Reduction in medullary concentrating gradient/ ADH antagonism effects
- osmotic diuresis, chronic renal impairment, post obstructive nephropathy, metabolic - hypocalcaemia/ hyponatremia, renal infiltration - amyloid
Familial
1. X linked V2 receptor defect
2. Autosomal - aquaporin defect

32
Q

Investigations for DI?

A
  1. Water deprivation- normally concentrates urine

2. Desmopressin IM for differentiation - will concentrate Cranial DI

33
Q

Managing cranial DI?

A
  1. Treat underlying condition

2. Give synthetic ADH analogue - oral desmopressin

34
Q

Managing nephrogenic DI?

A

More difficult

1. Avoid precipitating drugs e.g. tetracycline and lithium, NSAIDs, thiazide

35
Q

Congenital DI treatment?

A

Difficult

  1. Access to water
  2. High dose desmopressin
36
Q

Clinical presentation of moderate hyponatraemia?

A
  1. Headache
  2. Irritability
  3. Confusion
  4. Drowsy/Disoriented
  5. Nausea/vomiting
  6. Mental slowing
37
Q

Clinical presentation of severe hyponatraemia?

A
  1. Stupor/coma
  2. Convulsions
  3. Respiratory arrest
38
Q

Clinical presentation of SIADH?

A
  1. Varied/ generic
  2. Anorexic/nausea
  3. Weakness/aches
  4. Confusion/drowsiness
  5. Fits/comas
39
Q

Causes of SIADH?

A
  1. CNS : head injury, meningitis, encephalitis
  2. Resp : pneumonia, severe asthma, tuberculosis
  3. Tumours: carcinoma, sarcoma, leukaemia
  4. Metabolic: alcohol withdrawal
  5. Drugs: carbamazepine, thiazides, desmopressin
40
Q

How much can sodium increase by over 24 hours when treating SIADH?

A

Make sure not more than 8mmol/l due to risk of central pontine myelinosis

41
Q

Brain adaptations with onset of hyponatraemia?

A
  1. Water gain
  2. Rapid decrease in Na K Cl to shrink brain
  3. Slow loss of organic osmolytes
    These both contribute to loss of water
42
Q

What is improper treatment of hypotonic state?

A

Rapid correction

43
Q

Consequence of improper therapy?

A

Osmotic demyelination

44
Q

Risk factors for osmotic demyelination?

A
  1. Low serum Na+
  2. Hypokalaemia
  3. Chronic excess alcohol
  4. Malnutrition
  5. Advance liver disease
  6. Rapid increase in serum Na+
45
Q

Managing acute severe hyponatraemia?

A
  1. IV 150ml of 3% saline or equivalent over 20 mins
  2. Check serum Na+
  3. Repeat until increase in Na+ = 5mmol/l
  4. Don’t let increase >10mmol/l
46
Q

What are Vaptans?

A

v2 receptor anatagonist treating euvolaemic/hypervolaemic hyponatraemia

47
Q

Which part of pancreas produce digestive enzymes? What enzymes?

A
  1. Acinar cells = responsible for producing digestive enzymes e.g. amylase, lipase, colipase, phospholipase and proteases
48
Q

What do enterochromaffin cells secrete?

A

Serotonin production

49
Q

Aetiology of acute pancreatitis?

A 
Idiopathic
Gallstones
Ethanol - alcohol
Trauma
Steroids 
Measles/Mumps
Autoimmune disease
Scorpion venom
Hyperlipidaemia
ERCP
Drugs - thiazides, valproate
\+pregnancy, neoplasia
50
Q

Which of the aetiologies of acute pancreatitis causes ductal obstruction?

A
  1. Gallstones
  2. Ethanol
  3. ERCP
  4. Neoplasia
51
Q

Which of the aetiologies of acute pancreatitis causes acinar cell injury?

A
  1. Alcohol
  2. Trauma
  3. Drugs
52
Q

Which of the aetiologies of acute pancreatitis causes defective intracellular transport?

A
  1. Alcohol
  2. Autoimmune
  3. Hyperlipidaemia
53
Q

Pathophysiology of acute pancreatitis?

A

Accumulation of enzyme rich fluid and increased intracellular Ca2+ leads to early activation of trypsinogen which is cleaved to trypsin –> build –> digestion of pancreas and inflammation

54
Q

Symptoms of acute pancreatitis?

A

Severe epigastric pain radiating to the back

Nausea/vomiting

55
Q

Signs of acute pancreatitis?

A

Mild pyrexia

  1. Tachycardia
  2. Jaundice
  3. Periumbilical bruising or flanks due to blood vessel autodigestion and retroperitoneal haemorrhage
56
Q

How to diagnose acute pancreatitis?

A
  1. Serum amylase - 3 times the upper limit of normal
  2. Serum lipase - more specific
  3. FBC, U&E, glucose, CRP
  4. Erect CXR: exclude other causes e.g. gastroduodenal perforation
  5. CT with contrast enhancement
  6. Abdominal US - detect gallstone, swollen pancreas, dilated CBD and free peritoneal fluid
  7. MRI - severity, oedema
57
Q

Acute pancreatitis management?`

A
  1. Severity assessment
  2. Analgesia - pethidine/ IV benzodiazepine
  3. Catheterise and ABC approach for shock
  4. Fluid resuscitate if necessary
  5. Drain oedematous fluid
  6. Antibiotics
  7. Nutrition - orally if not vomiting/other inabilities
58
Q

What is SIRS defined by?

A
  1. T <36/>38
  2. HR >90bpm
  3. RR >20/min
  4. WBC <4 x109/L or >12)
59
Q

Define chronic pancreatitis?

A

Irreversible fibrosis of pancreatic parenchyma accompanied by calcification and dilation of pancreatic ducts.

60
Q

Causes of chronic pancreatitis?

A
  1. Genetic mutations - cystic fibros/ defects in trypsinogen gene
  2. Alcohol + smoking
  3. Autoimmune/ haemochromatosis
  4. Idiopathic/pancreatic duct obstruction
  5. CKD, raised PTH
61
Q

What may be raised serology wise in chronic pancreatitis?

A
  1. IgG4
62
Q

How to diagnose chronic pancreatitis?

A
  1. Blood - FBC, U&E, creatinine, LFT, calcium, amylase
  2. Imaging: US/ upper GI endoscopy
  3. Confirm with CT - look for calcification
  4. MRCP
63
Q

Managing chronic pancreatitis?

A
  1. Analgesia - opiates for sever pain in controlled environmnet
  2. Treat underlying cause
    Cessation of smoking, alcohol
    Diabetes - Insulin
    Malabsorption - replace enzymes
64
Q

Autoimmune chronic pancreatitis managment ?

A

Steroid responsive - 4-6 weeks oral prednisolone

Phase 2 Mine (12 decks)

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