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Endocrinology Flashcards

(40 cards)

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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

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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

Study These Flashcards
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

Study These Flashcards
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

Study These Flashcards
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

Study These Flashcards
A

Tachycardia

Fever

AF

Heart failure

Diarrhoea

Vomiting

Dehydration

Jaundice

Agitation

Delirium

Coma

22
Q

Treatment of thyroid crisis

Study These Flashcards
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

Study These Flashcards
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?

Study These Flashcards
A

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

Low TSH <0.4, normal T3/T4

25
**Causes** of **hypothyroidism**
_**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
**Treatment** for **hypothyroidism** (incl. dose and timing)
**Levothyroxine 50-100mcg** taken at least 30 mins before breakfast/caffeine/other drugs
27
**Features** of **myoedema coma** (incl. blood results)
Features of hypothyroidism Hyperthermia Coma Seizures _Bloods_: Raised TSH, low T3/4, hyponatraemia, raised CK
28
**Treatment** of **myxoedema coma**
**IV T4** **IV hydrocortisone 100mg** Fluids Correct electrolyte disturbances Antibiotics if likely infection
29
**Management** of **T1DM**
**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
**Complications** of **T1DM**
**_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
**Symptoms** and **definition** of **hypoglycaemia**
**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
**Treatment** of **hypoglycaemia**
_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
**Cause** of **T2DM**
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
**Complications** of **T2DM**
* 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
Type 2 diabetes is likely in a person who presents with:
* **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
To **dx T2DM** need
**HbA1c of 48+mmol/L** (on 2 occasions if asymptomatic or 1 if symptomatic) ## Footnote **Random plasma glucose \>11mmol/L**
37
**Management** of **T2DM**
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
**Fetaures** and **investigations** for **diabetes insipidus**
_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
What causes **diabetes insipidus** and what are the 2 major forms?
A condition caused by **hyposecretion of, or insensitivity to the effects of, antidiuretic hormone** ## Footnote _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
**Management** of **diabetes insipidus**
Cranial: desmopressin Nephrogenic: rehydration, correct electrolyte abnormalities, stop drugs which may be causing problem/ DDAVP. Combo of thiazide diuretic + NSAID may reduce urine volume.

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