Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

2a > endo > Flashcards

endo Flashcards

1
Q

What is Type 1 Diabetes Mellitus?

A

Autoimmune destruction of pancreatic beta cells leading to complete insulin deficiency.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the risk factors for Type 1 Diabetes?

A
  • HLA DR3-DQ2 or HLA DR4-DQ8
  • Northern European
  • Autoimmune disease - 90%
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the epidemiology of Type 1 Diabetes?

A
  • Usually presents ages 5-15
  • 10% of diabetes = T1DM
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How do you make a Type 1 Diabetes diagnosis?

A

Random plasma glucose > 11mmol/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What causes Type 2 Diabetes?

A

Reduced insulin secretion +/- increased insulin resistance
Others: Gestational Diabetes, Steroids, Cushing’s, Chronic pancreatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the symptoms and signs of Type 2 Diabetes?

A
  • Polydipsia
  • Polyuria
  • Glycosuria
  • Central obesity
  • Slower onset
  • Blurred vision
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is DPP4?

A

Depeptidyl peptidase
Part of the 2nd line management for Type 2 Diabetes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is Diabetic ketoacidosis?

A

Complete lack of insulin results in high ketone production
Medical emergency - serious complication of T1DM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the aetiology of Diabetic ketoacidosis?

A
  • Untreated or undiagnosed T1DM
  • Infection/illness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the signs of Diabetic ketoacidosis?

A
  • Kussmaul’s breathing
  • ‘Pear drop’ breath
  • Hypotension
  • Tachycardia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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+
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the treatment for Diabetic ketoacidosis?

A
  1. ABC management
  2. Replace fluid - 0.9% saline IV
  3. IV insulin
  4. Restore electrolytes - eg. K+
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Why would breathing change in Diabetic ketoacidosis?

A

DKA = Metabolic acidosis = results in respiratory compensation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is Hyperosmolar hyperglycaemic state?

A
  • Marked hyperglycaemia
  • Hyperosmolality
  • Mild/no ketosis
    Medical emergency - serious complication of T2DM
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is the aetiology of Hyperosmolar hyperglycaemic state?

A
  • Untreated or undiagnosed T2DM
  • Infection/illness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is the pathophysiology of Hyperosmolar hyperglycaemic state?

A

Low insulin -> increased gluconeogenesis -> hyperglycaemia, but enough insulin to inhibit ketogenesis
Hyperglycaemia -> osmotic diuresis -> dehydration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What are the symptoms and signs of Hyperosmolar hyperglycaemic state?

A

Extreme diabetes symptoms
PLUS:
- Confusion and reduced mental state
- Lethargy
- Severe dehydration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

How should you investigate Hyperosmolar hyperglycaemic state?

A
  • Random plasma glucose >11mmol/L
  • Urine dipstick: glucosuria
  • Plasma osmolality - high
  • U+E - ↓ total body K+, ↑ serum K+
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is the treatment for Hyperosmolar hyperglycaemic state?

A
  • Replace fluid - 0.9% saline IV
  • Insulin - At low rate of infusion!
  • Restore electrolytes - e.g. K+
  • LMWH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Why does Hyperosmolar hyperglycaemic state require a low insulin infusion rate?

A

High sensitivity to insulin
Risk of causing cerebral oedema glucose is lowered too quickly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is Hyperthyroidism?

A

Clinical effect of excess thyroid hormone
- Primary - abnormal ↑ thyroid function
- Secondary abnormal ↑ TSH production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is the aetiology of Hyperthyroidism?

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is the epidemiology of Hyperthyroidism?

A
  • Mainly young women - 20-40 yrs
  • Grave’s disease 0.5% prevalence
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What are the risk factors for Hyperthyroidism?

A
  • Smoking
  • Stress
  • HLA-DR3
  • Other autoimmune diseases: T1DM, Addisons, Vitiligo
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is the pathophysiology of Hyperthyroidism?

A

↑ T3 increases metabolic rate, cardiac output, bone resorption and activates sympathetic nervous system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is the result of mild and moderate iodine deficiencies?

A

Multifocal autonomous growth of thyroid, which results in thyrotoxicosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What are the symptoms and signs of Hyperthyroidism?

A

Everything goes fast!
- Hot + sweaty
- Diarrhoea
- Hyperphagia (excessive eating)
- Weight loss
- Palpitations
- Tremor
- Irritability
- Anxiety/restlessness
- Oligomenorrhoea (irregular periods)
- Goitre

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What is GOITRE?

A

A lump or swelling at the front of the neck caused by a swollen thyroid.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

How should you investigate Hyperthyroidism?

A
  • TFTs - ↑T4/T3, Primary: ↓TSH, Secondary: ↑TSH
  • Thyroid autoantibodies (anti-TSHR)
  • US + CT head
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What is the treatment for Hyperthyroidism?

A
  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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What is the pathophysiology of Graves Disease?

A

IgG autoantibodies (anti-TSHR-Ab) bind to TSH receptors to increase T4/T3 production
They also react with orbital autoantigens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What are the additional symptoms of Graves Disease?

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What are the most important things to remember about Graves Disease?

A

GravEs = HypErthyoidism = Eyes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What is thyroid acropachy?

A

Clubbing, painful finger + toe swelling, periosteal reaction (bone growth)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What is Hypothyroidism?

A

Clinical effect of lack of thyroid hormone
- Primary - abnormal ↓ thyroid function
- Secondary - abnormal ↓ TSH production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What is the epidemiology of Hypothyroidism?

A
  • 4/1000 per year
  • Mainly >40 years old
  • F>M - 6:1
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What is the pathophysiology of Hypothyroidism?

A

Not enough T3 to increase metabolic rate for normal body functions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What is the aetiology of Hypothyroidism?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What are the most important things to remember about Hypothyroidism?

A

HashimOtos = HypOthyroidism = slOw

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What is the Wolff-Chaikoff effect?

A

Mechanism for iodine excess causing hypothyroidism (unclear)
Excess iodine results in inhibition of thyroid hormone synthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What are the symptoms and signs of Hypothyroidism?

A

Everything goes slow!
- Fatigue
- Weight gain
- Loss of appetite cold
- Lethargy
- Constipation
- Low mood/depression
- Menorrhagia (abnormally heavy periods)
- Goitre

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

How should you investigate Hypothyroidism?

A

TFTs - ↓T4 ↓T3, Primary: ↑TSH, Secondary ↓ TSH
Autoantibodies (anti-TPO)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What is the treatment for Hypothyroidism?

A

Levothyroxine (T4)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What are the signs of Hypothyroidism?

A

Think BRADYCARDIC:
Bradycardia
Reflexes
Ataxia
Dry hair/skin
Yawning
Cold hands
Ascites
Round face (puffy)
Defeated demeanour
Immobile
Congestive cardiac failure

55
Q

What is Cushing’s Syndrome?

A

Long term exposure to excessive cortisol hormone which is released by adrenal glands.

56
Q

What causes Cushing’s Syndrome?

A

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
Q

What is the difference between Cushing’s Disease and Cushing’s Syndrome?

A

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
Q

What are the symptoms and signs of Cushing’s Syndrome?

A
  • Moon face
  • Central obesity
  • Buffalo hump
  • Acne
  • Hypertension
  • Striae
  • Hirsutism (essentially male-like facial hair in females)
  • Weight gain
59
Q

How should you investigate Cushing’s Syndrome?

A
  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
Q

What is the treatment for Cushing’s Syndrome?

A

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
Q

What is Acromegaly?

A

Release of excess growth hormone (GH) causing overgrowth of all systems

62
Q

What are the causes of Acromegaly?

A
  • Pituitary Adenoma = most common (99%)
  • Secondary to a malignancy that secrete ectopic GH eg. lung cancer
63
Q

What is the pathophysiology of Acromegaly?

A

GH acts directly on tissues such as liver, muscle bone or fat, as well as indirectly through induction of insulin like growth factor.

64
Q

What are the complications of Acromegaly?

A

Erectile dysfunction, Diabetes Mellitus

65
Q

What is the most common cause of Acromegaly?

A

Excessive growth hormone secretion from a pituitary tumour

66
Q

What are the symptoms and signs of Acromegaly?

A
  • 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
Q

What are the classic signs of Acromegaly that you can ask the patient about?

A
  • Ask to see older pictures of patient to see facial changes
  • Ask about ring and shoe size changing
68
Q

How should you investigate Acromegaly?

A
  • 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
Q

What is the treatment for Acromegaly?

A
  • 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
Q

What is the difference between the 1st line and gold standard investigations for Acromegaly?

A

Testing growth hormone - not reliable as levels very throughout the day for normal people and increases when stressed, pregnant, puberty

71
Q

What is Prolactinoma?

A

Benign adenoma of pituitary gland producing excess Prolactin

72
Q

What causes Prolactinoma?

A

Unknown
Some genetic association

73
Q

Besides Prolactinoma, what else can cause Hyperprolactinaemia?

A
  • Non functioning pituitary tumour - compresses pituitary stalk -> no inhibition of prolactin release
  • Antidopaminergic drugs
74
Q

What is the pathophysiology of Prolactinoma?

A

Increased release of prolactin can cause galactorrhoea by stimulating milk production from mammary gland, as well as inhibiting FSH and LH

75
Q

What are the 2 types of Prolactinoma?

A

Micro (tumour less than 10mm diameter on MRI; most common - 90%)
Macro (tumour more than 10mmm diameter on MRI)

76
Q

What are the symptoms and signs of Prolactinoma?

A
  • Visual field defect
  • Headache
  • Menstrual irregularity
  • Infertility
  • Galactorrhoea
77
Q

How should you investigate Prolactinoma?

A
  • Prolactin levels
  • CT head
78
Q

What is the treatment for Prolactinoma?

A
  • Gold standard: Transsphenoidal resection surgery of pituitary gland
  • 1st line: Dopamine agonists: bromocriptine/cabergoline (Dopamine has an inhibitory effect on prolactin)
79
Q

What are some additional consequences of Prolactinoma?

A

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
Q

What is Conn’s Syndrome?

A

Primary hyperaldosteronism due to an aldosterone producing adenoma.

81
Q

What is the pathophysiology of Conn’s Syndrome?

A

Excess production of aldosterone, independent of renin-angiotensin system =
- High Sodium and water retention
- Increased potassium excretion in kidneys
- Low renin release

82
Q

What are the symptoms and signs of Conn’s Syndrome?

A

Hypertension
Hypokalaemia
Nocturia
Polyuria
Mood disturbance
Difficulty concentrating

83
Q

How should you investigate Conn’s Syndrome?

A

Aldosterone-Renin Ratio blood test: Increased
Plasma potassium: reduced
U+E

84
Q

What is the treatment for Conn’s Syndrome?

A
  • 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
Q

What is Addison’s Disease?

A

Primary adrenal insufficiency

86
Q

What is the pathophysiology of Addison’s Disease?

A

Destruction of adrenal cortex leads to decreased production of glucocorticoid (cortisol) and mineralocorticoid (aldosterone)

87
Q

What causes Addison’s Disease?

A

Autoimmune destruction (80% in UK and developed countries)
TB (most common cause worldwide)
Adrenal metastases

88
Q

What are the symptoms and signs of Addison’s Disease?

A

OFTEN DIAGNOSED LATE
- Tanned
- Lean
- Fatigue
- Pigmented palmar creases
- Postural hypotension

89
Q

How should you investigate Addison’s Disease?

A

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
Q

What further tests can be done to investigate Addison’s Disease?

A

Adrenal CT or MRI
21-Hydroxylase adrenal autoantibodies - is positive in autoimmune disease in more than 80%

91
Q

What is the treatment of Addison’s Disease?

A

Replace steroids depending on signs + symptoms:
- Hydrocortisone - replaces cortisol
- Fludrocortisone - replaces aldosterone
Treat underlying cause and warn against abruptly stopping steroids

92
Q

What is Syndrome of Inappropriate ADH (SIADH)?

A

Inappropriately large amounts of ADH secretion causing water to be reabsorbed in collecting duct.

93
Q

What causes Syndrome of Inappropriate ADH?

A

Post-operative from major surgery
Infection (atypical pneumonia + lung abscess)
Head injury
Medications (thiazide diuretics) is most common cause

94
Q

What are the symptoms and signs of Syndrome of Inappropriate ADH?

A

NON-SPECIFIC:
- Headache
- Nausea
- Fatigue
- Muscle cramps
- Confusion
- Severe hyponatraemia

95
Q

How should you investigate Syndrome of Inappropriate ADH?

A

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
Q

What is the management for Syndrome of Inappropriate ADH?

A

Treat underlying cause:
- Stop causative medication
- Fluid restriction
- Tolvaptan (ADH receptor blocker)

97
Q

What is Hyperkalaemia?

A

> 5.5mmol/L

98
Q

What is the aetiology of Hyperkalaemia?

A

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
Q

What is metabolic acidosis?

A

Cells switch H+ for K+ to reduce acidosis

100
Q

What is tumour lysis?

A

Intracellular contents released

101
Q

What are the symptoms of Hyperkalaemia?

A

Fatigue and light-headedness
Weakness
Chest pain
Palpitations

102
Q

What are the signs of Hyperkalaemia?

A

Arrythmias (potential cardiac arrest)
Reduced power + reflexes
Flaccid paralysis
Signs of the underlying cause

103
Q

How does Hyperkalaemia appear on an ECG?

A
  • Small/absent P waves
  • Prolonged PR interval (>200ms)
  • Wide QRS interval (>120ms)
  • Tall tented T waves
104
Q

How should you investigate Hyperkalaemia?

A

ECG
Bloods - FBC, U+E
Urine osmolality and electrolytes

105
Q

What is the treatment for Hyperkalaemia?

A
  • ABC
  • Cardiac monitoring
  • Calcium gluconate - to protect myocardium
  • Insulin + Dextrose or Nebulised salbutamol - drive K+ intracellularly
  • Treat underlying cause
106
Q

What is Hypokalaemia?

A

<3.5mmol/L

107
Q

What is the aetiology of Hypokalaemia?

A

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
Q

What are the symptoms of Hypokalaemia?

A
  • Asymptomatic
  • Fatigue and light-headedness
  • Weakness
  • Cramps
  • Palpitations
  • Constipation
109
Q

What are the signs of Hypokalaemia?

A
  • Arrhythmias
  • Hypotonia
  • Hyporeflexia
  • Muscle paralysis
  • Rhabdomyolysis
110
Q

How does Hypokalaemia appear on an ECG?

A

Prolonged PR interval
ST depression
Flat T waves
Prominent U waves

111
Q

How should you investigate Hypokalaemia?

A

ECG
Bloods - FBC, U+E
Urine osmolality and electrolytes

112
Q

What is the treatment for Hypokalaemia?

A
  • Potassium - PO/IV
  • Other electrolytes as required
  • Treat underlying cause
113
Q

What are the 2 types of Diabetes insipidus?

A
  1. Cranial
  2. Nephrogenic
114
Q

What are the symptoms of Diabetes insipidus?

A

Polyuria
Polydipsia
Dehydration

115
Q

What is the pathophysiology of Diabetes insipidus?

A

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
Q

What are the causes of Cranial Diabetes insipidus?

A
  • Idiopathic
  • Congenital
  • Tumour
  • Trauma
  • Infection
117
Q

What are the causes of Nephrogenic Diabetes insipidus?

A
  • Inherited
  • Metabolic (low potassium, high calcium)
  • Drugs (lithium)
  • Chronic renal disease
118
Q

How can you make a diagnosis of Diabetes insipidus?

A

Gold standard - 8 hour water deprivation test to diagnose
Then Desmopressin test = establish cranial or nephrogenic
OTHER INVESTIGATIONS: cranial MRI

119
Q

What is the treatment for Diabetes insipidus?

A

Underlying cause
- Managed conservatively - mild cases - rehydration
- Cranial: Desmopressin (synthetic ADH) to replace ADH
- Nephrogenic: if cause persists, give Bendroflumethiazide

120
Q

What is Hyperparathyroidism?

A

Excessive secretion of Parathyroid Hormone (PTH)

121
Q

What are the 3 types of Hyperparathyroidism?

A
  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
Q

What are the causes of Hyperparathyroidism?

A

Primary: Adenomas (80%)
Secondary: CKD/Low Vit D
Tertiary: develops from prolonged secondary hyperparathyroidism

123
Q

What are the symptoms and signs of Hyperparathyroidism?

A

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
Q

What does Parathyroid Hormone (PTH) do?

A

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
Q

How should you investigate Hyperparathyroidism?

A

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
Q

What is the bone ‘salt and pepper sign’?

A

Multiple tiny well-defined lucencies (glowing/giving off light) in the bone caused by resorption or trabecular bone in hyperparathyroidism.

127
Q

What is the management for Hyperparathyroidism?

A

Watchful waiting
- Primary: Surgical removal or adenoma, give Bisphosphonates
- Secondary: calcium correction, treat underlying cause
- Tertiary: Cinacalcet (calcium mimetic), total/part parathyroidectomy

128
Q

What is Hypoparathyroidism?

A

Reduced PTH production
Primary - gland failure
- Autoimmune destruction
- Congenital - DiGeroge syndrome (22q11 del)
Secondary
- Surgical removal
- ↓Mg (required for PTH secretion)

129
Q

What are the risk factors for Hypoparathyroidism?

A

Other autoimmune disorders

130
Q

What is the pathophysiology of Hypoparathyroidism?

A

Low PTH results in
- Hypocalcaemia
- Hyperphosphatemia
Neurons become more excitable

131
Q

What are the symptoms of Hypoparathyroidism?

A

“CATS go numb”
Convulsions
Arrhythmias
Tetany (intermittent muscle spasms)
Spasm
Numbness

132
Q

What are the signs of Hypoparathyroidism?

A

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
Q

How should you investigate Hypoparathyroidism?

A

Bloods - bone profile
- ↓ Ca2+
- ↑ /normal Phosphate
- ↓ PTH
ECG
- Prolonged QT + ST segments

134
Q

What is the treatment for Hypoparathyroidism?

A

IV Calcium
AdCal D3 - Calcitriol
Synthetic PTH if required

2a (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions