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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Co-morbidities of acromegaly?

A
Hypertension
Cardiovascular events 
Headache
Arthritis
Insulin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Symptoms of acromegaly

A
Headache
Acral enlargement
Excess sweating
Visual deterioration
Increased weight
Amenorrhoea
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Signs of acromegaly

A
Rings too tight
Jaw prognathism
Coarser face
Darker pigmentation
Deep voice
Fatigue
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Diagnosis of acromegaly

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is Addison’s disease?

A

Adrenal insufficiency - destruction of the adrenal cortex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Causes of hypoadrenalism?

A
  1. Autoimmune adrenalitis
  2. TB
  3. Amyloid infiltration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Symptoms of Addison’s disease?

A
  1. weight loss
  2. fatigue
  3. poor recovery from illness
  4. headache
  5. adrenal crisis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Signs of Addison’s disease?

A
  1. Hyperpigmentation
  2. Hypotension
  3. Low Na+, high K+
  4. Eosinophilia
  5. Borderline elevated TSH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How to treat adrenal insufficiency?

A
  1. Hydrocortisone
  2. Primary: fludrocortisone oral - replace mineralocorticoids
  3. Carry steroid card and bracelet
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Symptoms of adrenal crisis?

A
  1. Fatigue
  2. Vascular collapse
  3. Dehydration
  4. Renal shut down
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Signs of adrenal crisis?

A
  1. Hyponatraemia/Hyperkalaemia
  2. Hypotension/CVD collapse
  3. Fatigue
  4. Fever
  5. Hypoglycaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Causes of secondary adrenal insufficiency?

A

Hypopituitarism

  1. Pituitary macroadenoma
  2. Apoplexy
  3. Hypophysitis
  4. Metastases, infiltration, infection
  5. radiotherapy
  6. congenital
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Craniopharyngioma presentation

A
  1. Visual field defects
  2. Hypopituitarism
  3. Raised ICP
  4. Growth failure
  5. Weight increase
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Rathke’s cyst presentation

A
  1. Headache
  2. Amenorrhea
  3. Hypopituitarism
  4. Hydrocephalus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Meningioma presentation

A
  1. Visual field defects
  2. Loss of visual acuity
  3. Endocrine dysfunction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Electrolytes present in the ECF

A

Na+, Cl-, HCO3-

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Common electrolytes in ICF

A

Potassium, magnesium, phosphate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Exogenous solutes that may affect osmolality?

A
  1. Alcohol
  2. Methanol
  3. Polythene
  4. Glycol
  5. Manitol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Output drivers of water?

A
  1. Excretion by kidney controlled by GFR and vasopressin

2. Uncontrolled insensible losses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Calculation for osmolality?
2Na+ + glucose + urea
26
What is cranial DI
Decreased vasopressin. Secreted from posterior pituitary
27
Nephrogenic DI?
Impaired response to action of vasopressin
28
Differential diagnosis of DI?
Hyperglycaemia Hypercalcaemia Hypokalemia
29
Diagnosis of DI?
1. Urinary volume>3L/day 2. Check renal volume and serum calcium 3. Plasma osmolality <300 4. Hyponatremia 5. Water deprivation test
30
Causes of cranial DI?
``` 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
Causes of nephrogenic DI?
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
Investigations for DI?
1. Water deprivation- normally concentrates urine | 2. Desmopressin IM for differentiation - will concentrate Cranial DI
33
Managing cranial DI?
1. Treat underlying condition | 2. Give synthetic ADH analogue - oral desmopressin
34
Managing nephrogenic DI?
More difficult | 1. Avoid precipitating drugs e.g. tetracycline and lithium, NSAIDs, thiazide
35
Congenital DI treatment?
Difficult 1. Access to water 2. High dose desmopressin
36
Clinical presentation of moderate hyponatraemia?
1. Headache 2. Irritability 3. Confusion 4. Drowsy/Disoriented 5. Nausea/vomiting 6. Mental slowing
37
Clinical presentation of severe hyponatraemia?
1. Stupor/coma 2. Convulsions 3. Respiratory arrest
38
Clinical presentation of SIADH?
1. Varied/ generic 2. Anorexic/nausea 3. Weakness/aches 4. Confusion/drowsiness 5. Fits/comas
39
Causes of SIADH?
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
How much can sodium increase by over 24 hours when treating SIADH?
Make sure not more than 8mmol/l due to risk of central pontine myelinosis
41
Brain adaptations with onset of hyponatraemia?
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
What is improper treatment of hypotonic state?
Rapid correction
43
Consequence of improper therapy?
Osmotic demyelination
44
Risk factors for osmotic demyelination?
1. Low serum Na+ 2. Hypokalaemia 3. Chronic excess alcohol 4. Malnutrition 5. Advance liver disease 6. Rapid increase in serum Na+
45
Managing acute severe hyponatraemia?
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
What are Vaptans?
v2 receptor anatagonist treating euvolaemic/hypervolaemic hyponatraemia
47
Which part of pancreas produce digestive enzymes? What enzymes?
1. Acinar cells = responsible for producing digestive enzymes e.g. amylase, lipase, colipase, phospholipase and proteases
48
What do enterochromaffin cells secrete?
Serotonin production
49
Aetiology of acute pancreatitis?
``` Idiopathic Gallstones Ethanol - alcohol Trauma Steroids Measles/Mumps Autoimmune disease Scorpion venom Hyperlipidaemia ERCP Drugs - thiazides, valproate +pregnancy, neoplasia ```
50
Which of the aetiologies of acute pancreatitis causes ductal obstruction?
1. Gallstones 2. Ethanol 3. ERCP 4. Neoplasia
51
Which of the aetiologies of acute pancreatitis causes acinar cell injury?
1. Alcohol 2. Trauma 3. Drugs
52
Which of the aetiologies of acute pancreatitis causes defective intracellular transport?
1. Alcohol 2. Autoimmune 3. Hyperlipidaemia
53
Pathophysiology of acute pancreatitis?
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
Symptoms of acute pancreatitis?
Severe epigastric pain radiating to the back | Nausea/vomiting
55
Signs of acute pancreatitis?
Mild pyrexia 2. Tachycardia 3. Jaundice 4. Periumbilical bruising or flanks due to blood vessel autodigestion and retroperitoneal haemorrhage
56
How to diagnose acute pancreatitis?
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
Acute pancreatitis management?`
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
What is SIRS defined by?
1. T <36/>38 2. HR >90bpm 3. RR >20/min 4. WBC <4 x109/L or >12)
59
Define chronic pancreatitis?
Irreversible fibrosis of pancreatic parenchyma accompanied by calcification and dilation of pancreatic ducts.
60
Causes of chronic pancreatitis?
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
What may be raised serology wise in chronic pancreatitis?
1. IgG4
62
How to diagnose chronic pancreatitis?
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
Managing chronic pancreatitis?
1. Analgesia - opiates for sever pain in controlled environmnet 2. Treat underlying cause Cessation of smoking, alcohol Diabetes - Insulin Malabsorption - replace enzymes
64
Autoimmune chronic pancreatitis managment ?
Steroid responsive - 4-6 weeks oral prednisolone