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PA > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What are the features of DKA?

A

Abdo pain

Polyuria, polydipsia, dehydration

Kussmaul respiration (deep hyperventilation)

Pear drop breath

Confusion

High glucose, ketones ++

Low pH and bicarb

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2
Q

What is the diagnostic criteria for DKA?

A

Glucose >11mmol/L or known diabetic

pH <7.3

Ketones >3mmol/L or ++ in urine

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3
Q

What is the management of DKA?

A

IV 0.9% NaCl Insulin infusion 0.1 unit/kg/hr (usually 5-8L depleted)!!

5% dextrose once BM <15 to prevent hypoglycaemia

Correct hypokalaemia

Continue LONG acting insulin, STOP SHORT acting

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4
Q

Causes of primary hyperparathyroidism

A

Adenoma

Hyperplasia

Carcinoma

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5
Q

Features of hyperparathyroidism

A

Features of hypercalcaemia!

Polydipsia, polyuria

Peptic ulceration/constipation/pancreatitis

Bone pain/fracture

Renal stones

Depression

HTN

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6
Q

Blood results in primary hyperparathyroidism

A

Normal/High PTH

High Ca

Low phosphate

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7
Q

Pepperpot skull is characteristic of

A

Hyperparathyroidism

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8
Q

Management of primary hyperparathyroidism

A

Total parathyroidectomy- definitive

Conservative if Ca <0.25, patient >50yrs and no end-organ damage

Calcimimetic agents e.g. cincalet if unfit for surgery

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9
Q

Causes of Addisonian crisis

A

Sepsis

Surgery

Adrenal haemorrhage (Waterhouse-Friderichsen syndrome)

Steroid withdrawal

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10
Q

Management of Addisonian crisis

A

IV 0.9% saline

Hydrocortisone IV/IM 100mg

If hypoglycaemic give 20% dextrose

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11
Q

Symptoms/signs of Addisonian crisis

A

Nausea/vomiting

Severe fatigue

Severe headache

Mental confusion

Hypotension causing postural hypotension

Hyponatraemia

Hyperkalaemia

Hypoglycaemia

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12
Q

Investigations for Addisonian crisis

A

FBC U&Es, LFT, glucose, lipase

Capillary glucose

Venous blood gas

If suspected NEW dx take random cortisol and ACTH

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13
Q

Investigations for Addison’s disease

A

ACTH stimulation test (short synacthen test)

No response = hypoadrenalism

  1. Take basal sample for cortisol
  2. Give 250mcg Synacthen IV or IM
  3. Sample for cortisol taken @ 30 mins & 60 mins
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14
Q

Features of Addisons

A

Fatigue

Hyperpigmentation (sun-exposed areas, pressure points, mucous membranes, palmar creases, areas of friction, recent scars)

GI Sx- weight loss/anorexia/premature saiety/N/V/abdo pain

Muscle weakness, cramps, joint pain

Postural dizziness

Headache, fever, increased thirst/urination, loss of axillary/pubic hair in women, delayed puberty

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15
Q

Raised cortisol

A

Cushing’s

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16
Q

Cushings disease vs Cushings syndrome

A

Cushings syndrome = raised cortisol due to either raised cortisol alone or raised ACTH causing the raised cortisol.

A pituitary tumour causing raised cortisol is Cushing’s Disease

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17
Q

Cushing’s features

A

Central obesity/Cervical fat pads/Collagen weakness/Comedones (acne)

Urinary free cortisol + glucose ↑

Striae/Supressed immunity

Hypercortisolism/Hypertension/Hyperglycaemia/Hirsutism

Neoplasms

Glucose ↑

Metabolic acidosis and hyperkalaemia + hyperpigmentation if raised ACTH

18
Q

Investigations for Cushing’s

A

ACTH (↑or↓) and cortisol (↑)

Dexamethasone suppression test (low dose then high dose).

  • Cortisol decreased at high dose= Cushing’s Disease.
  • Not reduced= Cushing’s syndrome.

Urinary free cortisol 24hr (↑) CT/MRI to establish cause

19
Q

Treatment for Cushing’s

A

Depends on the cause

Remove cause- stop steroids/surgery if tumour/remove adrenal gland

Metyrapone (inhibits cortisol synthesis)

Ketoconazole

20
Q

Causes of hyperthyroidism

A

Primary:

  • Graves- most common cause. TSH-R Abs, autoimmune. Goitre. Eye signs in 30% (proptosis, lid lag)
  • Toxic multinodular goitre - associated with iodine deficiency, more common in >60s. Benign folliclular adenoma.
  • Toxic thyroid nodule (adenoma)
  • Drugs e.g. iodine in amiodarone or contrast medium

Secondary:

  • Raised hCG (pregnancy)
  • Pituitary adenoma secreting excess TSH (rare)
  • Thyroid hormone resistance

Causes of thyrotoxicosis without hyperthyroidism:

  • Drugs- levothyroxine excess gives TSH <0.1
  • Thyroiditis:
    • Postpartum
    • Acute (bacterial infection)
    • Subacute (DeQuervains)- painful thyroid, fever, viral infection.
21
Q

Clinical features of thyroid storm

A

Tachycardia

Fever

AF

Heart failure

Diarrhoea

Vomiting

Dehydration

Jaundice

Agitation

Delirium

Coma

22
Q

Treatment of thyroid crisis

A

Treat precipitating cause e.g. infection

O2, IV access, 0.9% saline, NG tube if vomiting

Antithyroid treatment:

carbimazole or propylthiouracil

Beta blockers (propanolol 5mg IV) or diltiazem

Hydrocortisone

23
Q

Treatment for hyperthyroidism

A
  • Drug treatment:
    • carbimazole 1st line- titration block (titrate dose depending on T4), or block and replace (levothyroxine added when T4 normal)
  • Radioiodine treatment
  • Total or near-total thyroidectomy
24
Q

Management of subclinical hyperthyroidism

+ what would TFTs show?

A

Repeat TFTs 3-6 months if other causes of low TSH ruled out and asymptomatic

Low TSH <0.4, normal T3/T4

25
Q

Causes of hypothyroidism

A

Primary:

  • Overt (Raised TSH, low T4):
    • Autoimmune e.g. Hashimotos (goitre), atrophic (no gotire)- Thyroid peroxidase antibodies
    • Iodine deficiency
    • Drugs e.g. carbimazole, propylthiouracil
  • Subclinical (raised TSH, normal T3/4)

Secondary:

Due to pituitary/hypothalamic disorder= insufficient production of bioactive TSH

26
Q

Treatment for hypothyroidism

(incl. dose and timing)

A

Levothyroxine 50-100mcg taken at least 30 mins before breakfast/caffeine/other drugs

27
Q

Features of myoedema coma

(incl. blood results)

A

Features of hypothyroidism

Hyperthermia

Coma

Seizures

Bloods: Raised TSH, low T3/4, hyponatraemia, raised CK

28
Q

Treatment of myxoedema coma

A

IV T4

IV hydrocortisone 100mg

Fluids

Correct electrolyte disturbances

Antibiotics if likely infection

29
Q

Management of T1DM

A

DAFNE

Insulin- 1st line is multiple injection basal bolus regimen- basal twce daily detemivir plus bolus of rapid acting insulin analogue before meals

(alternative is twice daily human mixed insulin regimen e.g. humulin)

Monitor for complications

30
Q

Complications of T1DM

A

Microvascular

  • Nephropathy- kidney damage causing CKD
  • Retinopathy
  • Painful neuropathy
  • Autnomic neuropathy (sweating, postural hypotension, gastroparesis, diarrhoea, erectile dysfunction)

Macrovascular

  • Cardiovascular disease
  • Cerebrovascular disease
  • Peripheral arterial disease

Metabolic

  • DKA
  • Dyslipidaemia

Psychologyical

Infections

Skin complications

Other autoimmune conditions e.g. thyroid disease, autoimmune gastritis/pernicious anaemia, coeliac, vitiligo, Addisons.

31
Q

Symptoms and definition of hypoglycaemia

A

Blood glucose <3.5mmol/L

Symptoms:

Mild- hunger, anxiety, irritability, palpitations, sweating, tingling lips

Weakness, lethargy, impaired vision, confusion, irrational behaviour

Severe- convulsions, LOC, coma

32
Q

Treatment of hypoglycaemia

A

Able to swallow:

  • 10-20g fast-acting carb e.g. sugary drink, glucose tablets, 4 jelly babies, 7 jelly beans, dextrogel
  • Recheck BM after 10-15 mins- if no response repeat above
  • When sx improve/normoglycaemia, increase carb at next meal (if meal due) or eat long acting starchy carb e.g. bread/pasta/potatoes

Unable to swallow:

  • IM glucagon (1mg)
  • Then oral carbohydate if responds and able to swallow within 10mins
  • Otherwise needs ambulance
33
Q

Cause of T2DM

A

a combination of insulin resistance (where the body is unable to respond to normal levels of insulin) and insulin deficiency (where the pancreas is unable to secrete enough insulin to compensate for this resistance)

34
Q

Complications of T2DM

A
  • Microvascular complications — retinopathy, nephropathy, and neuropathy.
  • Macrovascular complications — cardiovascular disease (CVD), cerebrovascular disease, and peripheral arterial disease (PAD).
  • Metabolic complications — dyslipidaemia and diabetic ketoacidosis (DKA, uncommon).
  • Psychological complications — including anxiety and depression.
  • Reduced quality of life.
  • Reduced life expectancy.
35
Q

Type 2 diabetes is likely in a person who presents with:

A
  • Hyperglycaemia — the characteristic features (thirst, polyuria, blurred vision, weight loss, recurrent infections, and tiredness) are not usually severe and may be absent.
  • Risk factor(s) for type 2 diabetes.
  • Evidence of insulin resistance (for example acanthosis nigricans).
  • No additional features of type 1 diabetes (such as rapid onset, often in childhood, insulin dependence, or ketoacidosis).
  • No features of monogenic diabetes or diabetes secondary to a pathological condition or disease, drug treatment, trauma, or pancreatic surgery.
36
Q

To dx T2DM need

A

HbA1c of 48+mmol/L (on 2 occasions if asymptomatic or 1 if symptomatic)

Random plasma glucose >11mmol/L

37
Q

Management of T2DM

A

Education- DESMOND programme, provide info

Lifestyle- healthy diet, exercise, stop smoking, avoid alcohol on empty stomach

Drugs:

1) Metformin
2) Add a gliptin/pioglitazone/sulfonuylurea/SGLT2i
3) metformin + 2 other anti-diabetic drugs, or start insulin
4) consider adding GLP-1 mimetic if BMI >35

38
Q

Fetaures and investigations for diabetes insipidus

A

Features

  • polyuria
  • polydipsia
  • high plasma osmolality, low urine osmolality

(a urine osmolality of >700 mOsm/kg excludes diabetes insipidus)

water deprivation test- deprive of fluids then give demsopressin

If responds to desmopressin is cranial DI

39
Q

What causes diabetes insipidus and what are the 2 major forms?

A

A condition caused by hyposecretion of, or insensitivity to the effects of, antidiuretic hormone

There are two major forms of DI:

Cranial DI: decreased secretion of ADH. Decreased secretion of ADH reduces the ability to concentrate urine and so causes polyuria and polydipsia.

Nephrogenic DI: decreased ability to concentrate urine because of resistance to ADH in the kidney.

40
Q

Management of diabetes insipidus

A

Cranial: desmopressin

Nephrogenic: rehydration, correct electrolyte abnormalities, stop drugs which may be causing problem/ DDAVP. Combo of thiazide diuretic + NSAID may reduce urine volume.

PA (12 decks)

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