endo Flashcards
1
Q
What is Type 1 Diabetes Mellitus?
A
Autoimmune destruction of pancreatic beta cells leading to complete insulin deficiency.
2
Q
What are the risk factors for Type 1 Diabetes?
A
- HLA DR3-DQ2 or HLA DR4-DQ8
- Northern European
- Autoimmune disease - 90%
3
Q
What is the epidemiology of Type 1 Diabetes?
A
- Usually presents ages 5-15
- 10% of diabetes = T1DM
4
Q
What is the pathophysiology of Type 1 Diabetes?
A
Autoantibodies attack beta cells in the islets of Langerhans -> Insulin deficiency -> hyperglycaemia
Continuous breakdown of glycogen from liver (gluconeogenesis) -> glycosuria
5
Q
What are the symptoms and signs of Type 1 Diabetes?
A
- Classic triad: Polydipsia, Polyuria, Weight-loss (BMI <25)
- Usually a short history of severe symptoms
- May also present with ketosis
6
Q
How do you make a Type 1 Diabetes diagnosis?
A
Random plasma glucose > 11mmol/L
7
Q
What is the treatment for Type 1 Diabetes?
A
- Insulin
- Short-acting insulins and insulin analogues - 4-6 hours
- Longer acting insulin - 12-24 hours
8
Q
Patient presents with: polydipsia, polyuria, ketosis, rapid weight-loss, young, BMI <25, personal or family history of autoimmune disease. What is most likely wrong with them?
A
New T1DM
9
Q
What is Type 2 Diabetes?
A
Non-insulin dependent
- Patients gradually become insulin resistant / pancreatic beta cells fail to secrete enough insulin or BOTH
- Progresses from impaired glucose tolerance
10
Q
What causes Type 2 Diabetes?
A
Reduced insulin secretion +/- increased insulin resistance
Others: Gestational Diabetes, Steroids, Cushing’s, Chronic pancreatitis
11
Q
What are the risk factors for Type 2 Diabetes?
A
- Lifestyle factors: obesity, lack of exercise, calorie and alcohol excess
- Higher prevalence in Asian men
- Above 40 yrs age - later onset
- Hypertension
12
Q
What are the symptoms and signs of Type 2 Diabetes?
A
- Polydipsia
- Polyuria
- Glycosuria
- Central obesity
- Slower onset
- Blurred vision
13
Q
How should you investigate Type 2 Diabetes?
A
- Fasting plasma glucose: more than 7 mmol/L
- Random plasma glucose more than 11 mmol/L
- HbA1c more than 48 mmol/L
14
Q
What is the 1st line management for Type 2 Diabetes?
A
Lifestyle changes
- Dietary advice: high in complex carbs, low in fat
- Smoking cessation
- Decrease alcohol intake
- Encourage exercise
- Regular blood glucose and HbA1c monitoring
15
Q
What is the 2nd line management for Type 2 Diabetes?
A
Medications
1. Metformin (biguanide): increases insulin sensitivity - first choice in overweight patients
2. If HbA1c remains high then dual therapy with metformin:
- DPP4 inhibitor
- Sulphonylurea (gliclazide) - increases insulin secretion
- Pioglitazone
3. If still high = triple therapy
4. Then insulin
16
Q
What is DPP4?
A
Depeptidyl peptidase
Part of the 2nd line management for Type 2 Diabetes
16
Q
What is Diabetic ketoacidosis?
A
Complete lack of insulin results in high ketone production
Medical emergency - serious complication of T1DM
17
Q
What is the aetiology of Diabetic ketoacidosis?
A
- Untreated or undiagnosed T1DM
- Infection/illness
18
Q
What is the pathophysiology of Diabetic ketoacidosis?
A
Absence of insulin -> uncontrolled catabolism -> unrestrained gluconeogenesis and decreased peripheral glucose uptake -> hyperglycaemia
Hyperglycaemia -> osmotic diuresis -> dehydration
Peripheral lipolysis for energy -> increase in circulating free fatty acids -> oxidised to Acetyl CoA -> ketone bodies (acidic) = Acidosis
19
Q
What are the symptoms of Diabetic ketoacidosis?
A
Extreme diabetes symptoms
PLUS:
- Nausea + vomiting
- Weight loss
- Confusion and reduced mental state
- Lethargy
- Abdominal pain
20
Q
What are the signs of Diabetic ketoacidosis?
A
- Kussmaul’s breathing
- ‘Pear drop’ breath
- Hypotension
- Tachycardia
21
Q
How should you investigate Diabetic ketoacidosis?
A
- Random plasma glucose >11mmol/L
- Plasma ketone >3mmol/L
- Blood pH <7.35 or Bicarb <15mmol/L
- Urine dipstick: glycosuria, ketonuria
- Serum U+E
- Raised urea + creatinine
- ↓ Total K+, ↑ Serum K+
22
Q
What is the treatment for Diabetic ketoacidosis?
A
- ABC management
- Replace fluid - 0.9% saline IV
- IV insulin
- Restore electrolytes - eg. K+
23
Q
Why would breathing change in Diabetic ketoacidosis?
A
DKA = Metabolic acidosis = results in respiratory compensation
24
What is Hyperosmolar hyperglycaemic state?
- Marked hyperglycaemia
- Hyperosmolality
- Mild/no ketosis
Medical emergency - serious complication of T2DM
25
What is the aetiology of Hyperosmolar hyperglycaemic state?
- Untreated or undiagnosed T2DM
- Infection/illness
26
What is the pathophysiology of Hyperosmolar hyperglycaemic state?
Low insulin -> increased gluconeogenesis -> hyperglycaemia, but enough insulin to inhibit ketogenesis
Hyperglycaemia -> osmotic diuresis -> dehydration
27
What are the symptoms and signs of Hyperosmolar hyperglycaemic state?
Extreme diabetes symptoms
PLUS:
- Confusion and reduced mental state
- Lethargy
- Severe dehydration
28
How should you investigate Hyperosmolar hyperglycaemic state?
- Random plasma glucose >11mmol/L
- Urine dipstick: glucosuria
- Plasma osmolality - high
- U+E - ↓ total body K+, ↑ serum K+
29
What is the treatment for Hyperosmolar hyperglycaemic state?
- Replace fluid - 0.9% saline IV
- Insulin - At low rate of infusion!
- Restore electrolytes - e.g. K+
- LMWH
30
Why does Hyperosmolar hyperglycaemic state require a low insulin infusion rate?
High sensitivity to insulin
Risk of causing cerebral oedema glucose is lowered too quickly
31
What is Hyperthyroidism?
Clinical effect of excess thyroid hormone
- Primary - abnormal ↑ thyroid function
- Secondary abnormal ↑ TSH production
32
What is the aetiology of Hyperthyroidism?
- Graves disease - 65-75%, Auto immune, F>M - 9:1
- Toxic multinodular goitre
- Toxic adenoma
- Metastatic follicular thyroid cancer
- Iodine excess (e.g. IV contrast)
- Secondary causes - TSH secreting pituitary tumour
33
What is the epidemiology of Hyperthyroidism?
- Mainly young women - 20-40 yrs
- Grave's disease 0.5% prevalence
34
What are the risk factors for Hyperthyroidism?
- Smoking
- Stress
- HLA-DR3
- Other autoimmune diseases: T1DM, Addisons, Vitiligo
35
What is the pathophysiology of Hyperthyroidism?
↑ T3 increases metabolic rate, cardiac output, bone resorption and activates sympathetic nervous system
36
What is the result of mild and moderate iodine deficiencies?
Multifocal autonomous growth of thyroid, which results in thyrotoxicosis
37
What are the symptoms and signs of Hyperthyroidism?
Everything goes fast!
- Hot + sweaty
- Diarrhoea
- Hyperphagia (excessive eating)
- Weight loss
- Palpitations
- Tremor
- Irritability
- Anxiety/restlessness
- Oligomenorrhoea (irregular periods)
- Goitre
38
What is GOITRE?
A lump or swelling at the front of the neck caused by a swollen thyroid.
39
How should you investigate Hyperthyroidism?
- TFTs - ↑T4/T3, Primary: ↓TSH, Secondary: ↑TSH
- Thyroid autoantibodies (anti-TSHR)
- US + CT head
40
What is the treatment for Hyperthyroidism?
1. Drug management
a. Beta-blockers - Rapid symptom relief
b. 1st line Carbimazole - Blocks synthesis of T4
c. 2nd line Propylthiouracil - Prevent T4->T3 conversion
2. Radioiodine
3. Thyroidectomy
41
What is the pathophysiology of Graves Disease?
IgG autoantibodies (anti-TSHR-Ab) bind to TSH receptors to increase T4/T3 production
They also react with orbital autoantigens
42
What are the additional symptoms of Graves Disease?
Hyperthyroidism symptoms
PLUS:
- Thyroid eye disease (25-50%)
○ Eyelid retraction
○ Periorbital swelling
○ Proptosis/Exophthalmos
- Pretibial myxoedema (plaques of thick, scaly skin and swelling of your lower legs)
- Thyroid acropachy (nail clubbing, swelling of digits and toes)
43
What are the most important things to remember about Graves Disease?
GravEs = HypErthyoidism = Eyes
44
What is thyroid acropachy?
Clubbing, painful finger + toe swelling, periosteal reaction (bone growth)
45
What is Hypothyroidism?
Clinical effect of lack of thyroid hormone
- Primary - abnormal ↓ thyroid function
- Secondary - abnormal ↓ TSH production
46
What is the epidemiology of Hypothyroidism?
- 4/1000 per year
- Mainly >40 years old
- F>M - 6:1
47
What is the pathophysiology of Hypothyroidism?
Not enough T3 to increase metabolic rate for normal body functions
48
What is the aetiology of Hypothyroidism?
Autoimmune causes
- Hashimotos (inflammation -> goitre). More common F 60-70 years old
- Primary atrophic hypothyroidism (atrophy -> no goitre)
Other primary - iodine deficiency, drugs (antithyroid drugs, iodine, lithium), post thyroidectomy/radioiodine
Secondary - hypopituitarism
49
What are the most important things to remember about Hypothyroidism?
HashimOtos = HypOthyroidism = slOw
50
What is the Wolff-Chaikoff effect?
Mechanism for iodine excess causing hypothyroidism (unclear)
Excess iodine results in inhibition of thyroid hormone synthesis
51
What are the symptoms and signs of Hypothyroidism?
Everything goes slow!
- Fatigue
- Weight gain
- Loss of appetite cold
- Lethargy
- Constipation
- Low mood/depression
- Menorrhagia (abnormally heavy periods)
- Goitre
52
How should you investigate Hypothyroidism?
TFTs - ↓T4 ↓T3, Primary: ↑TSH, Secondary ↓ TSH
Autoantibodies (anti-TPO)
53
What is the treatment for Hypothyroidism?
Levothyroxine (T4)
54
What are the signs of Hypothyroidism?
Think BRADYCARDIC:
Bradycardia
Reflexes
Ataxia
Dry hair/skin
Yawning
Cold hands
Ascites
Round face (puffy)
Defeated demeanour
Immobile
Congestive cardiac failure
55
What is Cushing's Syndrome?
Long term exposure to excessive cortisol hormone which is released by adrenal glands.
56
What causes Cushing's Syndrome?
ACTH dependent:
- Cushing's Disease-ACTH secreting from pituitary adenoma
- Ectopic ACTH production from small cell lung cancer
ACTH independent:
- Iatrogenic-Steroid use (most common)
- Adrenal adenoma
57
What is the difference between Cushing's Disease and Cushing's Syndrome?
Disease = refers to the specific condition where a pituitary adenoma (tumour) secretes excessive ACTH
Syndrome = refers to symptoms and signs that develop after prolonged abnormal elevation of cortisol
DISEASE -> SYNDROME (but NOT always the other way around!)
58
What are the symptoms and signs of Cushing's Syndrome?
- Moon face
- Central obesity
- Buffalo hump
- Acne
- Hypertension
- Striae
- Hirsutism (essentially male-like facial hair in females)
- Weight gain
59
How should you investigate Cushing's Syndrome?
1. Random plasma cortisol-raised
2. Overnight dexamethasone suppression test - cortisol will not be suppressed in Cushing's Disease
3. Urinary free cortisol (24 hr)
4. Plasma ACTH
60
What is the treatment for Cushing's Syndrome?
Depending on underlying cause
- Iatrogenic: stop medications if possible
- Cushing's disease: removal of pituitary adenoma = transsphenoidal surgery
- Adrenal adenoma: adrenalectomy
Cortisol synthesis inhibition:
- Metyrapone, Ketoconazole
61
What is Acromegaly?
Release of excess growth hormone (GH) causing overgrowth of all systems
62
What are the causes of Acromegaly?
- Pituitary Adenoma = most common (99%)
- Secondary to a malignancy that secrete ectopic GH eg. lung cancer
63
What is the pathophysiology of Acromegaly?
GH acts directly on tissues such as liver, muscle bone or fat, as well as indirectly through induction of insulin like growth factor.
64
What are the complications of Acromegaly?
Erectile dysfunction, Diabetes Mellitus
65
What is the most common cause of Acromegaly?
Excessive growth hormone secretion from a pituitary tumour
66
What are the symptoms and signs of Acromegaly?
- Prominent forehead and brow
- Increased jaw size
- Large hands, nose, tongue, feet
- Visual field defect (bitemporal hemianopia)
- Profuse sweating
- Lower pitch of voice
- Obstructive sleep apnoea
67
What are the classic signs of Acromegaly that you can ask the patient about?
- Ask to see older pictures of patient to see facial changes
- Ask about ring and shoe size changing
68
How should you investigate Acromegaly?
- 1st line: Insulin like Growth Factor 1 test - raised
- Gold standard: Oral glucose tolerance test
- Other tests: Random serum GH raised, MRI scan of pituitary fossa
69
What is the treatment for Acromegaly?
- 1st line: Transsphenoidal resection surgery (if cause is adenoma)
- 2nd line: Somatostatin analogue eg. Ocreotide
- 3rd line: GH receptor antagonist eg. Pegvisoment
- 4th line: Dopamine agonist eg. Cabergoline
70
What is the difference between the 1st line and gold standard investigations for Acromegaly?
Testing growth hormone - not reliable as levels very throughout the day for normal people and increases when stressed, pregnant, puberty
71
What is Prolactinoma?
Benign adenoma of pituitary gland producing excess Prolactin
72
What causes Prolactinoma?
Unknown
Some genetic association
73
Besides Prolactinoma, what else can cause Hyperprolactinaemia?
- Non functioning pituitary tumour - compresses pituitary stalk -> no inhibition of prolactin release
- Antidopaminergic drugs
74
What is the pathophysiology of Prolactinoma?
Increased release of prolactin can cause galactorrhoea by stimulating milk production from mammary gland, as well as inhibiting FSH and LH
75
What are the 2 types of Prolactinoma?
Micro (tumour less than 10mm diameter on MRI; most common - 90%)
Macro (tumour more than 10mmm diameter on MRI)
76
What are the symptoms and signs of Prolactinoma?
- Visual field defect
- Headache
- Menstrual irregularity
- Infertility
- Galactorrhoea
77
How should you investigate Prolactinoma?
- Prolactin levels
- CT head
78
What is the treatment for Prolactinoma?
- Gold standard: Transsphenoidal resection surgery of pituitary gland
- 1st line: Dopamine agonists: bromocriptine/cabergoline (Dopamine has an inhibitory effect on prolactin)
79
What are some additional consequences of Prolactinoma?
Secondary hypogonadism, reduced libido and sexual dysfunction in men.
Pituitary tumour is located near to the optic chiasm -> visual field disturbances.
Very rarely malignant.
80
What is Conn's Syndrome?
Primary hyperaldosteronism due to an aldosterone producing adenoma.
81
What is the pathophysiology of Conn's Syndrome?
Excess production of aldosterone, independent of renin-angiotensin system =
- High Sodium and water retention
- Increased potassium excretion in kidneys
- Low renin release
82
What are the symptoms and signs of Conn's Syndrome?
Hypertension
Hypokalaemia
Nocturia
Polyuria
Mood disturbance
Difficulty concentrating
83
How should you investigate Conn's Syndrome?
Aldosterone-Renin Ratio blood test: Increased
Plasma potassium: reduced
U+E
84
What is the treatment for Conn's Syndrome?
- 1st line: Spironolactone (pre-op controls BP and K+ levels) - if Hyperplasia
- Gold standard: Laparoscopic Adrenalectomy - if Adenoma
Aim is to lower BP, decrease aldosterone levels and resolve electrolyte imbalance
85
What is Addison's Disease?
Primary adrenal insufficiency
86
What is the pathophysiology of Addison's Disease?
Destruction of adrenal cortex leads to decreased production of glucocorticoid (cortisol) and mineralocorticoid (aldosterone)
87
What causes Addison's Disease?
Autoimmune destruction (80% in UK and developed countries)
TB (most common cause worldwide)
Adrenal metastases
88
What are the symptoms and signs of Addison's Disease?
OFTEN DIAGNOSED LATE
- Tanned
- Lean
- Fatigue
- Pigmented palmar creases
- Postural hypotension
89
How should you investigate Addison's Disease?
1st line: U+E = hyponatraemia, Hyperkalaemia, Blood glucose (hypoglycaemia)
Gold standard: Short SynACTHen test (ACTH stimulation test)
Presents with: Low cortisol, High ACTH
- Plasma renin and aldosterone - High renin, Low aldosterone
90
What further tests can be done to investigate Addison's Disease?
Adrenal CT or MRI
21-Hydroxylase adrenal autoantibodies - is positive in autoimmune disease in more than 80%
91
What is the treatment of Addison's Disease?
Replace steroids depending on signs + symptoms:
- Hydrocortisone - replaces cortisol
- Fludrocortisone - replaces aldosterone
Treat underlying cause and warn against abruptly stopping steroids
92
What is Syndrome of Inappropriate ADH (SIADH)?
Inappropriately large amounts of ADH secretion causing water to be reabsorbed in collecting duct.
93
What causes Syndrome of Inappropriate ADH?
Post-operative from major surgery
Infection (atypical pneumonia + lung abscess)
Head injury
Medications (thiazide diuretics) is most common cause
94
What are the symptoms and signs of Syndrome of Inappropriate ADH?
NON-SPECIFIC:
- Headache
- Nausea
- Fatigue
- Muscle cramps
- Confusion
- Severe hyponatraemia
95
How should you investigate Syndrome of Inappropriate ADH?
Is a diagnosis of exclusion
- U+E = hyponatraemia
- Urine sodium = high
- Urine osmolality = high
Causes of Hyponatraemia need to be excluded:
- -ve Short SynACTHen Test - exclude Adrenal insufficiency
- No diarrhoea, vomiting
- No history of diuretic use
- No AKI/CKD
96
What is the management for Syndrome of Inappropriate ADH?
Treat underlying cause:
- Stop causative medication
- Fluid restriction
- Tolvaptan (ADH receptor blocker)
97
What is Hyperkalaemia?
>5.5mmol/L
98
What is the aetiology of Hyperkalaemia?
Impaired Excretion:
AKI/CKD
Drug affect (ACEi, NSAIDS, Betablockers)
Renal tubular acidosis
Addison's disease (↓aldosterone)
Increase Intake:
IV K+ therapy
Increased dietary intake
Shift to Extracellular:
Metabolic acidosis - cells switch K+ for K+ to reduce acidosis
Rhabdomyolysis
Decreased insulin
Tumour lysis syndrome - intracellular contents released
99
What is metabolic acidosis?
Cells switch H+ for K+ to reduce acidosis
100
What is tumour lysis?
Intracellular contents released
101
What are the symptoms of Hyperkalaemia?
Fatigue and light-headedness
Weakness
Chest pain
Palpitations
102
What are the signs of Hyperkalaemia?
Arrythmias (potential cardiac arrest)
Reduced power + reflexes
Flaccid paralysis
Signs of the underlying cause
103
How does Hyperkalaemia appear on an ECG?
- Small/absent P waves
- Prolonged PR interval (>200ms)
- Wide QRS interval (>120ms)
- Tall tented T waves
104
How should you investigate Hyperkalaemia?
ECG
Bloods - FBC, U+E
Urine osmolality and electrolytes
105
What is the treatment for Hyperkalaemia?
- ABC
- Cardiac monitoring
- Calcium gluconate - to protect myocardium
- Insulin + Dextrose or Nebulised salbutamol - drive K+ intracellularly
- Treat underlying cause
106
What is Hypokalaemia?
<3.5mmol/L
107
What is the aetiology of Hypokalaemia?
Increased Excretion:
Renal disease
Drug effect (Thiazide, loop diuretics, laxatives)
GI loss (D+V)
Conns syndrome (↑aldosterone)
Decreased Intake:
Dietary deficiency or fasting
Liquorice abuse
Shift to Intracellular:
Metabolic alkalosis
Drug effect (Insulin, B2 agonists - SABAs and LABAs)
108
What are the symptoms of Hypokalaemia?
- Asymptomatic
- Fatigue and light-headedness
- Weakness
- Cramps
- Palpitations
- Constipation
109
What are the signs of Hypokalaemia?
- Arrhythmias
- Hypotonia
- Hyporeflexia
- Muscle paralysis
- Rhabdomyolysis
110
How does Hypokalaemia appear on an ECG?
Prolonged PR interval
ST depression
Flat T waves
Prominent U waves
111
How should you investigate Hypokalaemia?
ECG
Bloods - FBC, U+E
Urine osmolality and electrolytes
112
What is the treatment for Hypokalaemia?
- Potassium - PO/IV
- Other electrolytes as required
- Treat underlying cause
113
What are the 2 types of Diabetes insipidus?
1. Cranial
2. Nephrogenic
114
What are the symptoms of Diabetes insipidus?
Polyuria
Polydipsia
Dehydration
115
What is the pathophysiology of Diabetes insipidus?
Impaired water resorption from the kidneys:
- Large volumes of dilute urine because or reduced ADH
- Secretion from the posterior pituitary (Cranial)
OR
- Impaired response of the kidney to AH (Nephrogenic)
116
What are the causes of Cranial Diabetes insipidus?
- Idiopathic
- Congenital
- Tumour
- Trauma
- Infection
117
What are the causes of Nephrogenic Diabetes insipidus?
- Inherited
- Metabolic (low potassium, high calcium)
- Drugs (lithium)
- Chronic renal disease
118
How can you make a diagnosis of Diabetes insipidus?
Gold standard - 8 hour water deprivation test to diagnose
Then Desmopressin test = establish cranial or nephrogenic
OTHER INVESTIGATIONS: cranial MRI
119
What is the treatment for Diabetes insipidus?
Underlying cause
- Managed conservatively - mild cases - rehydration
- Cranial: Desmopressin (synthetic ADH) to replace ADH
- Nephrogenic: if cause persists, give Bendroflumethiazide
120
What is Hyperparathyroidism?
Excessive secretion of Parathyroid Hormone (PTH)
121
What are the 3 types of Hyperparathyroidism?
1. PRIMARY: 1 parathyroid gland produces excess PTH
2. SECONDARY: Increased secretion of PTH to compensate hypocalcaemia
3. TERTIARY: autonomous secretion of PTH even after correction of calcium deficiency, due to Chronic Kidney Disease (CKD)
122
What are the causes of Hyperparathyroidism?
Primary: Adenomas (80%)
Secondary: CKD/Low Vit D
Tertiary: develops from prolonged secondary hyperparathyroidism
123
What are the symptoms and signs of Hyperparathyroidism?
BONES - bone pain
STONES - renal calculi
MOANS - psychic moans (NEUROPSYCHIATRIC, effects of nervous system: lethargy, fatigue, memory loss, psychosis, depression)
GROANS - abdominal groans (NAUSEA)
Hypercalcaemia
124
What does Parathyroid Hormone (PTH) do?
PTH increases Calcium through bone resorption, gut absorption, renal reabsorption an activating Vit D
PTH raises calcium levels by releasing Calcium from your bones and increasing the amount of calcium absorbed from your small intestine. When blood0calcium levels are too high, the parathyroid glands produce less PTH.
125
How should you investigate Hyperparathyroidism?
PTH/bone profile: high PTH, high calcium low phosphates
PRIMARY: Raised calcium
SECONDARY: Low serum calcium, High PTH
TERTIARY: Raised calcium + raised PTH
DEXA scan, X ray (salt and pepper degradation of bone), ultrasound for stones
126
What is the bone 'salt and pepper sign'?
Multiple tiny well-defined lucencies (glowing/giving off light) in the bone caused by resorption or trabecular bone in hyperparathyroidism.
127
What is the management for Hyperparathyroidism?
Watchful waiting
- Primary: Surgical removal or adenoma, give Bisphosphonates
- Secondary: calcium correction, treat underlying cause
- Tertiary: Cinacalcet (calcium mimetic), total/part parathyroidectomy
128
What is Hypoparathyroidism?
Reduced PTH production
Primary - gland failure
- Autoimmune destruction
- Congenital - DiGeroge syndrome (22q11 del)
Secondary
- Surgical removal
- ↓Mg (required for PTH secretion)
129
What are the risk factors for Hypoparathyroidism?
Other autoimmune disorders
130
What is the pathophysiology of Hypoparathyroidism?
Low PTH results in
- Hypocalcaemia
- Hyperphosphatemia
Neurons become more excitable
131
What are the symptoms of Hypoparathyroidism?
"CATS go numb"
Convulsions
Arrhythmias
Tetany (intermittent muscle spasms)
Spasm
Numbness
132
What are the signs of Hypoparathyroidism?
Chvostek's sign - facial nerve tap induces spasm, tapping on facial nerve in the parotid gland region causes ipsilateral twitching of facial muscles
Trousseau's sign - BP cuff causes wrist flexion and fingers to pull together, carpopedal spasm caused by inflating BP cuff above systolic BP
133
How should you investigate Hypoparathyroidism?
Bloods - bone profile
- ↓ Ca2+
- ↑ /normal Phosphate
- ↓ PTH
ECG
- Prolonged QT + ST segments
134
What is the treatment for Hypoparathyroidism?
IV Calcium
AdCal D3 - Calcitriol
Synthetic PTH if required
