Endocrinology Flashcards

(47 cards)

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

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
What are some other causes of ACTH dependent causes of Cushing's syndrome
Ectopic ACTH production - small cell lung cancers (may also secrete ADH) - Carcinoid tumours Ectopic CRF production - medullary thyroid cancer and prostate cancer
26
What are the specific features of ectopic ACTH production
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
What are some ACTH independent causes (decreased ACTH due to negative feedback)
Adrenal adenoma/cancer - tumour is autonomous so dexamethasone suppression will have no effect Adrenal nodular hyperplasia - no dexamethasone suppression Iatrogenic - steroid use (common)
28
How does Cushing's syndrome present
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
What tests can be done for suspected cushings syndrome
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
How is Cushing's syndrome treated
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
What are the complications of an adrenalectomy
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
Which drugs can be given to lower cortisol levels before surgery for Cushing's syndrome
Metyrapone (blocks cortisol synthesis) | Ketoconazole (inhibits cytochrome p450 enzyme) and Fluconazole
33
What is Addison's disease
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
What are some of the causes of Addison's disease
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
How would Addisons disease present
``` 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
What would tests show in addisons disease
``` 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
In which situations may cortisol levels be falsely positive
Pregnancy and COCP - due to increase cortisol-binding globulin
38
How is Addison's disease treated
Replace steroids - 15-25mg hydrocortisone daily in 2-3 doses - Avoid giving late - may cause insomnia - mineralocorticoids to stop postural hypotension and electrolytes
39
What other management is involved in Addison's disease
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
What is secondary adrenal insufficiency caused by
Iatrogenic - long term steroid use leading to suppression of HPA axis only becomes apparent on withdrawal of steroids
41
What is primary hyperaldosteronism
excess production of aldosterone independent of the RAAS | Causing increased sodium and water retention and decreased renin release
42
How does primary hyperaldosteronism present
``` Often asymptomatic Sign of hypokalaemia - weakness - cramps - paraesthesiae - polyuria - polydipsia - BP increased - not always ```
43
What are the causes of Primary hyperaldosteronism
Solitary aldosterone producing adenoma - Conn's syndrome | Bilateral adrencorticol hyperplasia
44
How would you investigate a patient with suspected primary hyperaldosteronism
Bloods - FBC - U+Es - high sodium low potassium however not all pts have low K - Renin - low - Aldosterone - high
45
When should Conn's syndrome be suspected
Refractory hypertension e.g. despite 3 hypertensive drugs Hypertension with associated hypokalaemi Hypertension occurring before 40yrs of age esp in women
46
How is Conn's syndrome treated
Laparoscopic adrenalectomy and Spironolactone for 4 weeks pre op to control BP and K+
47
What causes secondary hyperaldosteronism
Due to high renin from reduced renal perfusion e.g. in renal artery stenosis, accelerated hypertension, diuretics, CCF or hepatic failure