Endocrinology Flashcards

1
Q

What is the pathophysiology of DKA

A

There is excessive glucose but cannot be taken up by the cells due to a lack of insulin
so the body metabolises proteins and fats into ketones for energy.
Ketones then cause a metabolic acidosis due to an excessive concentration of ketone anions in the blood

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2
Q

How may DKA present?

A
Gradual drowsiness 
vomiting and dehydration 
Polyuria 
Polydipsia
Lethargy
Anorexia 
non-specific abdominal pain 
Ketotic breath 
Coma 
Deep breathing - Kussmaul breathing
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3
Q

What are the triggers for DKA

A
Infection 
MI 
Pancreatitis
Chemo
antipsychotics 
Non-compliance 
Wrong Insulin dose
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4
Q

What are the three criteria needed for diagnosis of DKA

A
  1. Acidaemia (pH<7.3)
  2. Hyperglycemia
  3. Ketonaemia
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5
Q

What investigations are done in suspected DKA?

A

Bedside: Capillary blood glucose, urine dipstick, ECG
Bloods: blood glucose, FBC, U+Es, amylase, blood culture (if signs of infection), ketones
Imaging: CXR (may be considered)
ABG - for anion gap and pH

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6
Q

What type of anion gap will someone with DKA have?

A

High anion gap

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7
Q

How is the anion gap calculated?

A

(Na + K) - (Cl + HCO3)

shows if acidosis is metabolic

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8
Q

When would a patient with DKA be transferred to ICU?

A
high blood ketones 
low bicarb
a pH lower than 7.1 
Potassium lower than 3.5 
GCS <12
Sats <92
Systolic <90
Tachy or Brady 
Anion gap above 36
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9
Q

Why may potassium drop when insulin is given?

A

because insulin forces potassium back in the cells by increasing the sodium-potassium channel activity, therefore there is less within the blood causing hypokalaemia

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10
Q

When can ketonuria also occur?

A

After an overnight fast

Alcohol (if glucose is normal)

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11
Q

how is DKA managed?

A

if BP is low - 500ml bolus
Find out blood gases for pH, keones, glucose, bicarb, U+Es
50units of actrarapid into 49.5ml of 0.9% saline. Infuse at 0.1unit/kg/hr
Stat dose if infusion is delayed
Assess need for potassium replacement (if potassium falls below 5.5)
Catheterise
Consider NG tube if vomiting or drowsy

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12
Q

What should be considered once insulin is being administered

A
Glucose level
AVOID HYPOGLYCAEMIA 
once glucose drops below 14, start 10% glucose at 125ml/hr
Potassium level 
3.5-5.5 - Add 40mmol per litre of fluid 
<3,5 - Seek help from HDU/ICU
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13
Q

What is the typical fluid deficit in DKA?

A

100ml/kg

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14
Q

What are the complications of DKA?

A

Cerebral oedema (if sudden CNS decline get help) - if fluid and insulin given rapidly
Aspiration Pneumonia (drowsy/unconscious and vomiting)
Hypokalaemia - if potassium not replaced once insulin is given
Hypomagnesaemia
Hypophophataemia
Thromboembolism

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15
Q

Why is cerebral oedema a complication of DKA?

A

The high glucose content of the blood causes fluid to move from ICF to ECF therefore the cells in the brain shrink. If insulin and fluid is given to a patient in DKA too rapidly it cause a rapid reversal of osmolarity and fluid moves into the cells and causes cerebral oedema,

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16
Q

How does a hypoglycaemia present?

A

Rapid onset
Autonomic - sweating. anxiety, hunger, tremor, palpitations, dizziness
Neuroglycopenic - confusion, drowsiness, visual trouble, seizures, coma

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17
Q

What are the causes of hypoglycaemia?

A

EXPLAIN
Ex ogenous drugs e.g. insulin, oral hypoglycaemics, alcohol (binge without food) and aspirin poisoning
P ituitary insufficiency
L iver failure
A ddisons disease
I slet cell tumours
N on pancreatic neoplasms, e.g. fibrosarcomas

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18
Q

How is hypoglycaemia investigated?

A

BM
Bloods: glucose, FBC, U+Es, cortisol, insulin, c-peptide, plasma ketones
Drug history

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19
Q

What are the causes of hypoglycaemic hyperinsulinaemia?

A

Sulfonylureas, insulinoma, insulin injection (no detectable C peptide - only released with endogenous insulin)

20
Q

If the insulin is low and the plasma ketones are increased what are the differentials

A

Addisons disease
Pituitary insufficiency
Alcohol

21
Q

How is a hypoglycaemic episode treated?

A

Oral sugar and long acting starch
If cannot swallow - 25-50ml 50% glucose with 0.9%saline flush
Glucagon 1mg IM if not IV access (repeat after 20mins and follow with oral carb)

22
Q

What is Cushings Syndrome

A

Chronic state caused by excess glucocorticoids and loss of normal feedback mechanisms of HPA axis
exogenous - oral steroids
endogenous - increased secretion of cortisol (very rare)

23
Q

How is cortisol excreted

A

in the urine

24
Q

What are the causes of Cushings DISEASE?

A

ACTH secreting pituitary adenoma causing bilateral adrenal hyperplasia
A low dose dexamethasone test leads to no change in cortisol but 8mg may be enough to halve morning cortisol

25
Q

What are some other causes of ACTH dependent causes of Cushing’s syndrome

A

Ectopic ACTH production
- small cell lung cancers (may also secrete ADH)
- Carcinoid tumours
Ectopic CRF production - medullary thyroid cancer and prostate cancer

26
Q

What are the specific features of ectopic ACTH production

A

Increased ACTH production causes hyperpigmentation
Hypokalaemia
Metabolic alkalosis - increased mineralocorticoid activity - more odium retained and potassium excreted
Weight loss
Hyperglycaemia
Classical features of Cushing’s not usually present

27
Q

What are some ACTH independent causes (decreased ACTH due to negative feedback)

A

Adrenal adenoma/cancer - tumour is autonomous so dexamethasone suppression will have no effect
Adrenal nodular hyperplasia - no dexamethasone suppression
Iatrogenic - steroid use (common)

28
Q

How does Cushing’s syndrome present

A

Weight gain and central obesity
Moon face
buffalo neck hump
Acne
Mood change - depression, lethargy, irritability and psychosis
Proximal weakness
gonadal dysfunction - irregular menses, hirutisim, erectile dysfunction
MSK: recurrent achilles tendon rupture, osteoporosis
Skin: bruises, purple abdominal striae, poor healing
Infection-prone

29
Q

What tests can be done for suspected cushings syndrome

A

Random cortisol levels can be misleading due to time of day taken, stress and illness
24hr urinary cortisol secretion - increased cortisol
Overnight dexamethasone suppression test 1mg PO at midnight and serum cortisol done at 8am - no suppression Cushing’s syndrome
In Cushing’s disease there is 50% suppression in high dose (8mg) dexamethsone suppression
No suppression at high doses in ectopic disease

If the above normal
- 48hr dexamethasone suppression test - give 0.5mg PO 6hrly for 2 days - measure cortisol at 0 and 48hrs

30
Q

How is Cushing’s syndrome treated

A

Depends on cause
Iatrogenic: Stop steroids if possible, lower dose slowly
Cushing’s disease: selective removal of pituitary adenoma or bilateral adrenalectomy if source undetectable
Adrenal adenoma or carcinoma: adrenalectomy rarely cures cancer, radiotherapy and drugs follow if carcinoma
Ectopic ACTH: Surgery if tuour is located and hasnt spread

31
Q

What are the complications of an adrenalectomy

A

Nelsons syndrome - increase in skin pigmentation due to increase in ACTH from an enlarging pituitary tumour
Adrenals removed –> no negative feedback
Responds to pituitary radiation

32
Q

Which drugs can be given to lower cortisol levels before surgery for Cushing’s syndrome

A

Metyrapone (blocks cortisol synthesis)

Ketoconazole (inhibits cytochrome p450 enzyme) and Fluconazole

33
Q

What is Addison’s disease

A

Adrenal insufficiency - adrenal glands are unable to make enough cortisol for the body due to destruction of the adrenal cortex
Both glucocorticoid and mineralocorticoid deficiency

34
Q

What are some of the causes of Addison’s disease

A

Autoimmunity
TB - most common worldwide
Adrenal mets - from breast, lung and renal cell carcinoma
Lymphoma
Opportunistic infections in HIV - CMV, mycobacterium avium
Adrenal haemorrhage - Waterhour-Friderichsen syndrome, SLE, Antiphospholipid syndrome

35
Q

How would Addisons disease present

A
Very vague 
Often diagnosed late 
- lean 
-tanned 
- tired 
- weakness
- anorexia 
- Dizzy, faints, postural hypotension
- flu like myalgias/arthralgia 
GI: nausea/vomiting, abdo pain, diarrhoea/constipation 
Think of Addisons in unexplained abdominal pain or vomiting 
Skin: pigmented palmar creases/buccal mucosa, vitiligo
36
Q

What would tests show in addisons disease

A
Low sodium 
High potassium - due to decrease mineralocorticoid 
hypoglycaemia - due to reduced cortisol 
Also
- uraemia
- increased calcium 
- eosinophilia 
- anaemia 

Short Synacthen test: Do plasma cortisol before and 30mins after
Addisons excluded if 30mins cortisol is >550nmol/L

Plasma renin:aldosterone - asses mineralocorticoid status
21-hydroylase adrenal autoantibodies - positive in autoimmune disease >80%

Imaging
AXR/CXR - previous TB, calcification of adrenal glands

37
Q

In which situations may cortisol levels be falsely positive

A

Pregnancy and COCP - due to increase cortisol-binding globulin

38
Q

How is Addison’s disease treated

A

Replace steroids

  • 15-25mg hydrocortisone daily in 2-3 doses
  • Avoid giving late - may cause insomnia
  • mineralocorticoids to stop postural hypotension and electrolytes
39
Q

What other management is involved in Addison’s disease

A

Steroid Card
medic ID bracelet
Make doctors/surgeons/dentists aware if having treatment
Steroids need to be doubled in febrile illness, injury or stress
Give IM hydrocortisone and how to inject if vomiting prevents oral intake - seek medical help and admit for IV fluids if dehydrated

40
Q

What is secondary adrenal insufficiency caused by

A

Iatrogenic - long term steroid use leading to suppression of HPA axis
only becomes apparent on withdrawal of steroids

41
Q

What is primary hyperaldosteronism

A

excess production of aldosterone independent of the RAAS

Causing increased sodium and water retention and decreased renin release

42
Q

How does primary hyperaldosteronism present

A
Often asymptomatic 
Sign of hypokalaemia
- weakness
- cramps 
- paraesthesiae 
- polyuria 
- polydipsia 
- BP increased - not always
43
Q

What are the causes of Primary hyperaldosteronism

A

Solitary aldosterone producing adenoma - Conn’s syndrome

Bilateral adrencorticol hyperplasia

44
Q

How would you investigate a patient with suspected primary hyperaldosteronism

A

Bloods

  • FBC
  • U+Es - high sodium low potassium however not all pts have low K
  • Renin - low
  • Aldosterone - high
45
Q

When should Conn’s syndrome be suspected

A

Refractory hypertension e.g. despite 3 hypertensive drugs
Hypertension with associated hypokalaemi
Hypertension occurring before 40yrs of age esp in women

46
Q

How is Conn’s syndrome treated

A

Laparoscopic adrenalectomy and Spironolactone for 4 weeks pre op to control BP and K+

47
Q

What causes secondary hyperaldosteronism

A

Due to high renin from reduced renal perfusion e.g. in renal artery stenosis, accelerated hypertension, diuretics, CCF or hepatic failure