Endocrinology Flashcards
1
Q
What is the cause of acromegaly?
A
- Excessive secretion of growth hormone.
- Usually due to pituitary adenomas.
2
Q
Symptoms of acromegaly?
A
- Hands and feet enlargement
- Coarse facial features
- Macroglossia
- Enlargement of jaw (prognathism)
- DM2
- Hypertension
- Headaches
- Sweating
3
Q
What is the investigation done in acromegaly?
A
Initial test and for monitoring
- Insulin growth factor (IGF-1).
Confirmation of diagnosis
- Oral glucose test.
Others
- MRI scan of pituitary (adenomas).
4
Q
What is the treatment of acromegaly?
A
- Trans-sphenoidal surgery
- GH receptor antagonist: Pegvisomant
- Somatostatin analogues: octreotide
- Radiotherapy
5
Q
What is the physiology of Addison’s disease?
A
- AKA primary adrenal insufficiency;
- The adrenal gland (kidney) cannot produce adequate levels of cortisol (glucocorticoids) and aldosterone (mineralocorticoids) due to autoimmune destruction.
6
Q
What is the cause of primary Addison’s disease?
A
- Autoimmune.
7
Q
What are the symptoms of primary adrenal disease?
A
- Fatigue
- Weakness
- Weight loss
- Postural hypotension
- Hyperpigmentation (due to ACTH raised)
- Salt cravings
- Hypoglycaemia
8
Q
What are the investigations done in primary Addison’s disease?
A
- Electrolytes: Hyponatraemia & Hyperkalaemia.
- Early morning cortisol: low
- ACTH: high
- Synacthem / ACTH stimulation test: cortisol does not rise.
9
Q
What is the cause of SECONDARY adrenal insufficiency?
A
- Hypothalamic and pituitary failure.
- Long term steroid medication (suspension of hypothalamic-pituitary-adrenal axis)
10
Q
What is the investigation of secondary adrenal insufficiency?
A
- ACTH: low
- Cortisol (early morning): low
- ACTH stimulation test / Synacthem: cortisol does not rise.
11
Q
DDx between:
- Addison’s disease (primary adrenal insufficiency)
- Secondary adrenal insufficiency
A
• Primary adrenal insufficiency
- Autoimmune destruction of adrenal gland, leads to low cortisol and low aldosterone.
- Low cortisol leads to negative feedback to the pituitary which leads to high levels of ACTH which leads to hyperpigmentation.
- Low aldosterone leads to hyponatraemia and hyperkalaemia.
• Secondary adrenal insufficiency
- Inadequate pituitary or hypothalamic stimulation, leads to low ACTH, which leads to low cortisol.
- Aldosterone levels are normal hence normal Na and K.
12
Q
What is the DDx between:
- Conn’s syndrome
- Addison’s disease
A
Conn’s syndrome
- Hypernatraemia
- Hypokalaemia
- Hypertension
Addison’s disease
- Hyponatraemia
- Hyperkalaemia
- Hypotension
- Hypoglycaemia
13
Q
What are the causes of Addisonian crisis?
A
- Withdrawal of chronic steroid therapy
- Infection or stress (corticosteroids needs will be raised)
14
Q
What are the symptoms of Addisonian crisis?
A
- Shock: postural hypotension, tachycardia, oliguria
- Abdominal pain
- Hypoglycaemia
15
Q
What are the investigations of Addisonian crisis?
A
- Cortisol
- ACTH levels
- Blood sugar
- FBC, U&Es, Cultures
16
Q
What is the treatment of Addisonian crisis?
A
- IV hydrocortisone 100 mg
- IV fluids if shocked
- IV glucose if hypoglycaemia
- Improvement after 72h oral steroids
- If adrenal pathology identified: fludrocortisone.
17
Q
What is the Rx for DM₂?
A
First line:
- Metformin
Check HbA1c in 3-6 monthsIf HbA1c > 58 mmol/mol
- Reinforce lifestyle advice
- Add another drug.
If added cardiovascular risk:
- Metformin
AND
- SGLT-2 inhibitors
18
Q
DM2
Describe the adjustements of biguanides in relation to kidney injury.
A
Example: Metformin
Renal imparment adjustments- eGFR < 45: reduce dose- eGFR < 30: discontinue
19
Q
DM2
Describe the pharmacology of SGLT-2 inhibitors (AKA gliflozins).
A
Example:
- Dapagliflozin
- Canagliflozin
- Empagliflozin
Benefits
- Cardioprotective
- Renal protective
- Weight loss
Risks
- DKA at moderately raised glucose (< 14 mmol/L).
20
Q
DM2
Describe the pharmacology of Sulphonylurea.
A
Example:
- Gliclazide
Risks
- Hypoglycaemia
- Weight gain
Not to be given to lorry, ambulance, heavy machinery drivers due to hypoglycaemia.
21
Q
DM2
Describe the pharmacology of DDP4 inhibitors (AKA sitagliptin).
A
Example:
- Sitagliptin
Risks
- Pancreatitis
22
Q
DM2
Describe the pharmacology of Pioglitazone.
A
Contraindicated in:
- Heart failure
- Bladder cancer
- Fractures (women)
Risks
- Weight gain
23
Q
DM2
Describe the pharmacology of Repaglinide.
A
Risks
- Hypoglycaemia
- Weight gain
- Avoid in liver disease
24
Q
DDx between:
- Osteoporosis
- Paget’s disease
- Osteomalacia
A
Osteoporosis
Calcium: Normal
Phosphate: Normal
Alkaline phosphatase: Normal
Paget's disease
Calcium: Normal
Phosphate: Normal
Alkaline phosphatase: High
Osteomalacia
Calcium: Low
Phosphate: Low
Alkaline phosphatase: High
25
Define what is `Conn's syndrome / primary hyperaldosteronism`?
Condition due to excessive production of aldosterone by the adrenal glands.
26
What are the **symptoms** of `Conn's syndrome / primary hyperaldosteronism`?
- **Hypertension:** Due to ⬆︎ aldosterone ➝ hypernatraemia which causes water retention.
- **Hypokalaemia:** causes muscles weakness.
- **Hypernatraemia**
- **Metabolic alkalosis**
## Footnote
**Aldosterone** acts on the convulted tubules to:
- ↑ Na⁺ reabsortion
- ↑ K⁺ excretion
- ↑ H⁺ excretion
27
What is the **cause** of `Conn's syndrome / primary hyperaldosteronism`?
- Adrenal adenoma
- Adrenal hyperplasia
- Adrenal carcinoma
28
What are the **investigations** done in `Conn's syndrome / primary hyperaldosteronism`?
**Renim - Aldosterone ratio**
- `Renim: low`
- Aldosterone: High
**CT scan / MRI**
- Searching for adenomas, carcinomas, etc.
## Footnote
**Renim is low** because:
- The kidneys juxtaglomerular cells are responsible for sensing the BP coming to the kidneys.
- If the BP is low, they release renim
- Renim converts angioteninogem (produced by the liver) into angiotensin I
- Angiotensin 1 is then converted (in the lungs) into angiotensin 2 (by angiotensin converting enzymes)
- `Angiotensin 2 acts on the adrenal gland to produce aldosterone increasing the BP ➝ lowering renim`.
29
What is the **treatment** of `Conn's syndrome / primary hyperaldosteronism`?
**Aldosterone antagonist:**
- Spironolactone
**Surgery:**
- Adrenalectomy
30
Define what is `Cushing's syndrome`?
Condition caused by **prolongued exposure** of `endogenous or exogenous glucorticoids` leading to excessive cortisol on the body.
31
**Describe** the `adrenal axis physiology`.
1. *Hypothalamus* releases **CRH hormone**
2. *CRH* acts on the **anterior pituitary gland**
3. *Anterior pituitary* releases `ACTH hormone`
4. *ACTH* acts on the `adrenal gland`
5. *Adrenal gland* releases **`cortisol`**
6. *Cortisol* does the following:
◆ Inhibits the immune system;
◆ Inhibits bone formation;
◆ ⬆︎ blood glucose
◆ ⬆︎ metabolism
◆ ⬆︎ alertness
7. ⬆︎ Cortisol sends a negative feedback to the anterior pituitary and to the hypothalamus, and they ⬇︎ the production of their hormones.
32
What are the `causes` of **Cushings syndrome**?
◉ **`ACTH dependent disease`**
◆ ***Cushings disease***: Pituitary adenoma;
◆ ***Ectopic ACTH***: small lung carcinoma
◉ **`Non-ACTH dependent`**
◆ Adrenal adenoma/carcinoma
◆ Exogenous steroids
33
What are the `symptoms` of **Cushings syndrome**?
◆ Round face
◆ Buffalo hump
◆ Abdominal obesity
◆ Purple abdominal striae
◆ Muscle weakness
◆ Osteoporosis
◆ Depression and insomnia
34
How is the `diagnosis` of **Cushings syndrome** done?
## Footnote
**`Investigations done to diagnose it.`**
**1.** 24h urinary free cortisol;
**2.** Dexamethasone suppression test (low dose).
35
# Cushings syndrome
Explain how the **`low` dose dexa supression test** is done and its `clinical relevance`.
**1.** 1mg of Dexa is giving at midnight.
**2.** Cortisol (plasma) is measured the next day at 9 am.
➜ **If positive for Cushings:**
◆ 1mg of dexa `won't be enough` to supress the hypothalamus (CRH) or the anterior pituitary (ACTH), as the body is used to ⬆︎ levels of cortisol.
➜ **If negative for Cushings:**
◆ Cortisol < 50 nmol/L.
◆ 1mg of dexa `will be enough` to supress the hypothalamus and the anterior pituitary.
36
# Cushings syndrome
After `positive dexa supression test` (low dose), what is the next step?
◉ Differentiate the causes of Cushings by doing:
➜ **High dose dexamethasone supression test.**
37
Explain how the **`high` dose dexa supression test** is done and its `clinical relevance`.
`◘ 8mg of dexa is administered.`
➔ **Cushing disease/pituitary adenoma:**
◆ ACTH ⬇︎
◆ Cortisol ⬇︎
◆ 8 mg would supress the ACTH/adenoma
➔ **Adrenal adenoma:**
◆ ACTH ⬇︎
◆ Cortisol ⬆︎
◆ 8 mg would supress the pituitary but the source of the ↑ cortisol is on the kidney itself.
➔ **Ectopic ACTH (lung carcinoma):**
◆ ACTH ⬆︎
◆ Cortisol ⬆︎
◆ The source of the ↑ cortisol is elsewhere even though the pituitary is supressed.
38
# Diabetes
Describe the **Dawn phenomenom**.
It is a rise in glucose levels in the early hours (2 - 8 AM) in diabetic patients.
| Especially DM1.
39
# Diabetes
What is the **Rx** of the `Dawn phenomenom`?
⬆︎ night time dose of` long acting insulin`.
40
What is the **cause** of `diabetes insipidus`?
**1.** ⬇︎ production of ADH (antidiuretic hormone).
**2.** ⬇︎ response to ADH.
## Footnote
ADH is `produced by the hypothalamus` and `stored in the pitituitary`.
41
# Diabetes insipidus
What is the **function** of `ADH` (antidiuretic hormone)?
- Acts on the **collecting ducts** on the kidneys ⟶ `Reabsportion of H₂O from urine` *(urine becomes concentrated due to lack of water)*
**On diabetes insipidus:**
- ⬇︎ ADH
- Prevents urine from becoming concentrating due to excessive water in urine
- `Polyuria` (excessive amount of urine)
- `Polydipsia` (thirst caused by blood being concentrated)
42
What are the **symptoms** of `diabetes insipidus`?
- **Polyuria:** excessive amount of urine due to ⬆︎ water in the urine
- **Polydipsia:** thirst caused by blood being concentrated
43
What is the **classification** of `diabetes insipidus`?
**Nephrogenic:**
- Collecting ducts don't respond to ADH (resistance to ADH)
**Cranial:**
- ⬇︎ production of ADH by the hypoothalamus.
44
What are the **causes** of **`NEPHROGENIC`** `diabetes insipidus`?
**Nephrogenic:**
- Collecting ducts don't respond to ADH (resistance to ADH)
`- Example of causes:`
◆ Lithium
◆ Genetics
◆ Kidney disease
◆ Electrolyte imbalances (↓K⁺, ↑Ca⁺)
45
What are the **causes** of **`CRANIAL`** `diabetes insipidus`?
**Cranial:**
- ⬇︎ production of ADH by the hypoothalamus.
`- Example of causes:`
◆ Idiophatic
◆ Brain tumor
◆ Head injury
◆ Brain malformations
◆ Surgery
◆ Radiotheraphy
46
What is the **investigations** done in `diabetes insipidus`?
- **`Water deprivation test`**
- **Urine osmolality:** low (due to water excess)
- **Plasma osmolality:** high
47
Define what is **thyrotoxicosis**?
⬆︎ levels of the thyroid hormone in the body / plasma.
48
Define what is **Primary hyperthyroidism**?
It occurs when:
- The thyroid gland itself is responsible for ⬆︎ thyroid hormone production.
49
Define what is **Secondary hyperthyroidism**?
It occurs when:
- ⬆︎ levels of TSH released by the pituitary
- TSH will act on the thyroid hormone and ⬆︎ thyroid hormone production
## Footnote
The problem might be in the pituitary or the hypothalamus.
50
Describe what is **hyperprolactinaemia**.
⬆︎ levels of prolactin on the blood.
- Prolactin is produced by the anterior pituitary.
- It primarly regulates lactation.
51
Define what is **Graves disease**?
- Autoimune disease
- TSH receptor antibodies cause the hyperthyroidism
- These antibodies **mimic TSH** and `stimulate the TSH receptors on the thyroid`
- TSH receptors cause the thyroid gland to secrete ⬆︎ thyroid hormone.
52
Describe the **syndrome of galactorrhoea-amenorrhoea.**
- ⬆︎ ` prolactin levels` **⟶** prevents the hypothalamus from secreting luitenising hormone (LH) and follicle stimulating hormone (FSH) **⟶** `disruption of normal menstrual cycle` .
53
What are the `symptoms` of **Graves disease**?
- Exophtalmos
- Proptosis
- Eyelid lag
- Pretibial myxoedema
54
What are the `pathological causes` of **hyperprolactinaemia**?
- **Prolactinoma** (tumour)
- Hypothyroidism
- Antipsycotics: Risperidone, haloperidol, domperidone.
- Brain injury
55
What is the **treatment** of `Graves disease`?
**First line**
- Carbimazole
- Propylthiouracil
**Others**
- Radioiodine
- Thyroidectomy
56
What are the `symptoms` of **hyperprolactinaemia**?
**Females**
- Inhibition FSH & LH causes amenorrhoea and galactorrhoea
**Males**
- Secondary hypogonadism
- ⬇︎ libido
- Gynaecomastia
- Erectile dysfunction
**Neurological symptoms** (prolactinomas)
- Bilateral hemianopia
- Headaches
57
What are the **causes** of `hyperthyroidism`?
*`↑ T4 & ↓ TSH`*
**Causes**
`- Autoimmune (graves disease)`
- Toxic nodular goitre
- De Quervain's thyroiditis (infectious)
- Drugs (exogenous thyroid hormone)
58
What are the `investigations` done in **hyperprolactinaemia**?
- Prolactin level
- MRI (pituitary)
- Visual field testing
59
What is the `treatment` of **hyperprolactinaemia**?
**First line**
`Dopamine agonists`
- Cabergoline
- Bromocriptine
**Others**
-Surgery
- Radiotheraphy
60
What are the **symptoms** of `hyperthyroidism`?
**Gastro**
- ↑ appetite
- Weight loss
- Diarrhoea
**Cardio**
- Palpitations
- Tachycardia
**Others**
- Heat intolerance
- Oligomenorrhea
- Irritability
- Weakness
61
What is the **treatment** of `hyperthyroidism`?
*`↑ T4 & ↓ TSH`*
**First line**
- Carbimazole
- Propylthiouracil
**Others**
- Radioiodine
- Thyroidectomy
62
**DDx between:**
- Clinical hyperthyroidism
- Subclinical hyperthyroidism
`Clinical hyperthyroidism`
**T4:** High
**TSH:** Low
`Subclinical hyperthyroidism`
**T4:** Normal
**TSH:** Low
63
What are the **causes** of `thyrotoxic storm`?
- Radioidine (treatment)
- Thyroid surgery
- Myocardial infarction
- Infection
64
What are the **symptoms** of `thyrotoxic storm`?
- Altered mental status
- Coma
- Agitation
- Hyperthermia
- Atrial fibrillation
- Tachycardia
- Diarrhoea
- Vomiting
65
What are the **investigation** done in `thyrotoxic storm`?
- TSH
- T3
- T4
66
What is the **Rx** of `thyrotoxic storm`?
**Counteracting the peripheral effects of thyroid hormone**
- Beta blockade: propranol
- Digoxin (once adequately beta blocked)
**Inhibiting thyroid hormone synthesis**
- Propylthiouracil
- Lugol iodine
**Treat the causes**
## Footnote
Propylthiouracil prefered over carbimazole in emergencies as rapid onset.
67
What are the **causes** of `hypercalcaemia`?
- **Primary hyperparathyroidism**
- Malignancy (multiple myeoloma, bone metastasis)
- Sarcoidosis
- Hyperthyroidism
- Prolongued immobilization
- Thiazides
68
What are the **symptoms** of `hypercalcaemia`?
* **Gastro (Moans)**: Constipations due to ↓ bowel activity;
* **Renal (Stones)**: Kidney stones & nephrolithiasis due to calcium deposits in kidney. Polyuria & polydipsia due to induction of diabetic insipidus;
* **Neuro & Psych (Groans)**: Lethargy, confusion and depression;
* **Bone pain (Bones)**: seen in hyperthyroidism.
69
What is the management of **hypercalcaemia**?
1. Hydration with (3-4L) of NaCl 0.9% to induce urinary output and excretion of calcium;
2. Bisphosphonates IV (Zoledronic acid or pamidronate);
3. **In sarcoidosis**: steroids;
4. **2ry hyperparathyroidism**: Cinalcet hydrochoride;
5. **Renal failure**: hemodialysis;
70
DDx of **hypercalcaemia**?
**Primary hyperparathyroidism**
`Ca⁺:` `High`
`PTH:` `High`
**Secondary hyperparathyroidism**
`Ca⁺:` `Low`
`PTH:` `High`
**Primary hypoparathyroidism**
`Ca⁺:` `High`
`PTH:` `High`
**PTH independent hypercalcaemia**
`Ca⁺:` `High`
`PTH:` `Low`
71
What is the **classification** of `hyperparathyroidism`?
**1. Primary hyperparathyroidism**
**2. Secondary hyperparathyroidism**
**3. Tertiary hyperparathyroidism**
72
Explain the **physiology** of the `parathyroid glands`.
- There are **4 parathyroid glands** on the 4 corners of the thyroid gland.
- The parathyroid glands `function` is to `produce PTH hormone` in response to **`low serum Ca²⁺ levels`**.
- PTH ↑ Ca²⁺ reabsortion from the intestines, kidneys, and breaking down Ca²⁺ from the bones (to be released in the plasma)
◉ **VITAMIN D**
- Is a hormone produced by the body in response to sunlight and food.
- It acts on the intestines, kidneys and bones to increase the reabsortion of Ca²⁺.
- PTH also acts on vitamin D to enhace its action on Ca²⁺ reabsortion
## Footnote
Low Vit D causes hypocalcaemia.
73
Describe what is **primary hyperparathyroidism**:
- Causes
- Investigations
➜ Abnormal levels of PTH acts on the kidneys, guts and bones to ⬆︎ Ca²⁺ ➔ **`Hypercalcaemia`**.
**Causes:**
- Parathyroid adenoma
- Hyperplasia
- Carcinoma
**Investigations**
- ↑ PTH (could be normal)
- ↑ Ca²⁺
- ↓ Phosphate
## Footnote
PTH increases phosphate excretion by the kidneys.
74
Describe what is **secondary hyperparathyroidism**:
- Causes
- Investigations
➜ There is a `reduced` reabsortion of Ca²⁺ from the kidneys, guts and bones ➔ **`Hypocalcaemia`**.
**Causes:**
- ↓ Vitamin D
- CKD (there's abnormal absorption of Ca²⁺ in the guts due to ↓ production of an active form of Vit D by the kidneys).
**Investigations**
- ↑ PTH
- ↓ Ca²⁺ (could be normal)
- ↑ Phosphate in CKD
75
Describe what is **tertiary hyperparathyroidism**:
- Causes
- Investigations
➜ Occurs after prolongued 2ndary hyperparathyroidism.
➜ Hyperplasia of the glands occurs.
➜ ↑ baseline release of PTH
➜ After treatment of 2ndary hyperparathyroidism, the glands remain big and still secrete ⬆︎ levels of PTH ⟶ **`Hypercalcaemia`**.
**Causes:**
- Prolongation of 2nd hyperparathyroidism
**Investigations**
- ↑ PTH
- ↑ Ca²⁺
- ↑ Phosphate
76
What is the **Rx** for **secondary hyperparathyroidism**?
**Vitamin D supplementation**
- Cholecalciferol
- Alfacalcidol (in patients with severe renal impairment)
77
Describe what is **`pseudo`HYPOparathyroidism**:
Disorder where there is a resistance to PTH hormone in the body.
- Ca²⁺ will not get absorbed by the kidneys, gut and bones.
- Phosphate will not be excreted by the kidneys.
**Symptoms**
- ↓ Ca²⁺
- ↑ phosphate
- ⬆︎ PTH
## Footnote
PTH increases phosphate excretion by the kidneys.
78
**DDx** of:
- ALP (alkaline phosphatase)
- Ca²⁺
**⬆︎ ALP + ⬆︎Ca²⁺**
- Bone metastasis
- Hyperparathyroidism
**⬆︎ ALP + ⬇︎ Ca²⁺**
- Osteomalacia:
◆ Vit D deficiency
◆ Renal failure
◆ Anticonvulsants
79
Describe what is **hypothyroidism** and its classification.
Inadequate secretion of the thyroid hormones by the thyroid gland.
- `Primary hypothyroidism` (issue on the thyroid itself)
- `Secondary hypothyroidism` (insufficiency of TSH secretion by the pituitary/hypothalamus)
80
What are the **causes** of:
- `Primary HYPOthyroidism`
- `2ndary HYPOthyroidism`
**Primary hypothyroidism causes:**
- **`Autoimunne inflammation /. Hashimoto thyroiditis`**.
- Iodine deficiency (essential for T3, T4 production)
- Treatment for hyperthyroidism
- Lithium (inhibits T3, T4 production)
- Amiodarone
**Secondary hypothyroidism**
`- Pituitary disorder/Hypothalamic disorder:`
◆ Sheehans syndrome
◆ Tumors
◆ Radiation
81
What are the **labs features** of `hypothyroidism`?
**Primary hypothyroidism:**
- ⬆︎TSH
- ⬇︎T3, T4
**Secondary hypothyroidism**
- ⬇︎TSH
- ⬇︎T3, T4
82
What are the **symptoms** of `hypothyroidism`?
- Weight gain
- Cold intolerance
- Tiredness
- Dry skin
- Menstrual abnormalities
83
What is the **Rx** of **`hypothyroidism`**?
Levothyroxine.
84
What are the **features** of `SUBCLINICAL hypothyroidism`?
`- TSH High`
`- T4 normal`
**Primary hypothyroidism:**
- ⬆︎TSH
- ⬇︎T3, T4
**Secondary hypothyroidism**
- ⬇︎TSH
- ⬇︎T3, T4
85
What is the **management** of `SUBCLINICAL hypothyroidism`?
- Repeat blood tests in **3 - 6 months**.
**1. ⬆︎TSH but < 10 miU/L**
- On 2 tests 3 months apart
- Symptomatic
- < 65 years
`➜ Consider levothyroxine`
**2. ⬆︎TSH > 10 miU/L**
- On 2 tests 3 months apart
`➜ Consider levothyroxine`
86
What are the **causes** of `hypopituarism`?
➜ Lost of function of the pituitary gland
**Causes**
- `Pituitary adenoma`
- Sheehan's syndrome
- Tumous
- Infection
- Stroke
- Radiotheraphy
- Trauma
87
What are the **symptoms** of `hypopituarism`?
**`↓LH, ↓FSH`**
- Amenorrhoea
- Infertility
**`↓GH`**
- No symptoms in adults
**↓TSH**
- Hypothyroidism symptoms
**↓ACTH**
- Fatigue
- Hyponatraemia
- Hypotension
**↓Prolactin**
- Absent lactation
| 1st two are the main ones to be affected first.
88
Define **LADA** (latent autoimmune diabetes of adulthood)
A type of DM1 thar develops much slower and is diagnosed in adults.
89
# DM1
What is the investigation in LADA?
GAD antibody testing.
90
What is the **Rx** for ***hyperthyroidism*** in `pregnancy`?
**First trimester:**
- Propylthiouracil
**2nd and 3rd trimester:**
- Carbimazole
- Partial thyroidectomy if carbimazole is not effective.
**Postpartum:**
- Carbimazole
91
**DDx** between:
-Toxic nodular goitre
-Non-toxic goitre
**Toxic**
- Large goitre
- Produces ⬆︎ amount of thyroid hormones
**Non-toxic**
- Large goitre
- Produces **normal** amount of thyroid hormones.
92
**Rx** of:
-Toxic nodular goitre
-Non-toxic goitre
**Toxic**
1. FNAC: rule out malignancy
`2.` `Carbimazole`
`3. Radioidine: definitive treatment`
4. Thyroidectomy
**Non-toxic**
1. FNAC: rule out malignancy
`2. Thyroidectomy: if compression symptoms`
3. Radioidine: if surgery is not an option (elderly).
93
What are the ***symptoms*** and **labs** features of `osteomalacia`?
- **Bone pain**
- **Ca²⁺**: low
- **Serum phosphates:** low
- **ALP:** high
94
What is the **cause** and **treatment** for `Osteomalacia`?
- **Cause:** Vit D insufficiency, renal failure
- **Treatment:** calcium & vit D supplements
95
What are the **causes** of `osteoporosis`?
- Corticoisteroids (long term)
- Low BMI
- Premature menopause w/out Rx
- Immobillity
- Smoking
- Heavy alchool
96
In **osteoporosis**, what is the step by step management for `assessment and prevention`?
**Risk of osteoporosis**
1. Fracture risk assessment;
2. If risk ≥10% of osteoporotic; fracture than step 3;
3. Dexa scan;
4. T-score <-2.5 ➝ offer Rx.
**≥ 50 years & has a fragility fracture**
- Dexa scan
- T-score <-2.5 ➝ offer Rx.
97
# Osteoporosis
Describe Klinefelter syndrome.
- ⬇︎ bone mass and and density
- Caused by ⬇︎ testoterone levels.
**Treatment**
`- If ⬇︎ testosterone:` testotorene therapy
`- If not sure of cause:` Look for other cause, Vit D perhaps.
98
**DDx** between:
- Osteomalacia
- Osteoporosis
- Paget's disease
**`Osteoporosis`**
**- Ca²⁺:** normal
**- Serum phosphate:** normal
**ALP:** normal
**`Paget's disease`**
**- Ca²⁺:** normal
**- Serum phosphate:** normal
**ALP:** ⬆︎
**`Osteomalcia`**
**- Ca²⁺:** ⬇︎
**- Serum phosphate:** ⬇︎
**ALP:** ⬆︎
99
What is the **treatment** for `1ry hyperparathyroidism`?
**1.** Cinalcet
**2.** Bisphosphonates: if risk of fractures
**3.** Parathyroidectomy
100
What is the **treatment** for `prolactinomas`?
**Tumour < 10mm**
`Restore function with dopamine agonists`
- Cabergoline
- Bromocriptine
**Tumour > 10mm**
`1. Restore function with dopamine agonists`
- Cabergoline
- Bromocriptine
`2. Reduce tumour size`
- Surgery (if medical Rx fails)
101
Describe what is **Sheehan's syndrome**.
Necrosis of the pituitary gland secondary to massive haemorrhage and leading to hypopituitarism.
102
What are the `symptoms` of **Sheehan's syndrome**?
- Failure to lactate
- Amenorrhea / oligoamenorrhea
- Hypothyroidism
- Adrenal insufficiency
103
What are the `labs features` of **Sheehan's syndrome**?
**↓LH & ↓FSH**
- Failure to lactate and oligo/amenorrhea
**↓TSH, ↓T3, ↓T4**
- Hypothyroidism
**↓ACTH & ↓Cortisol**
- Adrenal insufficiency
104
What are the **labs features** of `SIADH secretion`?
| ADH is produced by the hypothalamus and stored in the pituitary.
## Footnote
Acts on the collecting ducts to induce water reabsorption.
**- ADH:** High
**- Urine osmolality:** High
**- Urine sodium:** High
**- Serum sodium:** Low
**- Plasma osmolality:** Low
105
What is the **Rx** of `SIADH secretion`?
- Treat the cause
- Fluids restriction (500 - 1L/24h)
- Demeclocycline (induces nephrogenic DI)
- Vaptans (in severe hyponatraemia)
