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2A > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What are the three ways hormones are distributed through?

A

Endocrine – blood-borne, acting at distant sites
Paracrine – acting on adjacent cells
Autocrine – feedback on same cell that secreted hormone

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2
Q

Features of water-soluble hormones

A

Transport - unbound
Cell interaction - bind to surface receptor
Half-life - short
Clearance - fast

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3
Q

Features of fat-soluble hormones

A

Transport - protein bound
Cell interaction - diffuse into cells
Half-life - long
Clearance - slow

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4
Q

What are the 4 classes of hormones?

A
  1. Peptides
  2. Amines
  3. Iodothyronines
  4. Cholesterol derivatives and steroids
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5
Q

What are the different mechanisms used to control hormone secretion?

A

Basal secretion – continuously or pulsatile

Superadded rhythms e.g day-night cycle – ACTH, prolactin, GH and TSH

Release inhibiting factors – dopamine inhibiting prolactin, sum of positive and negative effects (GHRH and somatostatin on GH)

Releasing factors

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6
Q

What hormones does the posterior pituitary synthesise?

A

NONE! Oxytocin and vasopressin (ADH) is stored in the posterior pituitary but is synthesised in the hypothalamus.

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7
Q

What would stimulate vasopressin release?

A

Vasopressin is an antidiuretic hormone. It is stimulated to absorb water from the kidney.

*Hypertonic concentration
*Loss of blood volume
*Stress

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8
Q

What does vasopressin do?

A

*Vasoconstricts blood vessels
*Increased release of aldosterone which leads to increased absorption of water
*Stimulates the release of ACH which in turn stimulates the release of cortisol

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9
Q

Where is oxytocin released?

A

Posterior pituitary gland

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10
Q

Function of oxytocin?

A
  1. Uterine contraction during labour.
  2. Milk ejection
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11
Q

What hormones are produced in the anterior pituitary gland and what are they stimulated by?

A

TSH - stimulated by TRH from hypothalamus
ACTH - stimulated by CRH from hypothalamus
FSH and LH - stimulated by GnRH from hypothalamus
GH - stimulated by GHRH from hypothalamus
PRL - inhibited by dopamine from hypothalamus

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12
Q

What are the three ways that someone with pituitary dysfunction would present?

A

*Tumour mass effects
*Hormone excess
*Hormone deficiency

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13
Q

What investigations should be conducted in patients with pituitary dysfunction?

A
  1. Make a clinical diagnosis
  2. Hormonal tests
  3. If hormonal tests abnormal or tumour mass effects perform MRI pituitary
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14
Q

When is oxytocin released?

A

It is stimulated by cervical dilation

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15
Q

Where does growth hormone act?

A

In the liver

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16
Q

What hormone does GH stimulate?

A

Insulin-like growth factors (IGFs)

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17
Q

Functions of thyroid hormone

A

*Accelerates food metabolism
*Increases protein synthesis
*Stimulation of carbohydrate metabolism
*Enhances fat metabolism
*Increase in ventilation rate
*Increase in cardiac output and heart rate
*Brain development during foetal life and postnatal development
*Growth rate accelerated

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18
Q

Main function of cortisol?

A

Major metabolic and stress hormone

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19
Q

Describe the structure of the adrenal gland.

A

Adrenal gland is divided into the medulla and cortex.
The cortex is made up of three layers:
GFR
*Zona glomerulosa
*Zona fasciculata
*Zona reticularis

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20
Q

Where in the adrenal cortex are mineralocorticoids produced and give an example of one.

A

Zona glomerulosa.| - Aldosterone.

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21
Q

Where in the adrenal cortex are glucocorticoids produced and give an example of one.

A

Zona fasciculata.| - Cortisol androgens

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22
Q

Where in the adrenal cortex are androgens produced and give an example of one.

A

Zona reticularis.| - androstenedione and DHEA

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23
Q

What is released by the adrenal medulla?

A

Epinephrine and norepinephrine

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24
Q

What happens in the zona glomerulosa

A

Renin-angiotensin system
*Low Na, sympathetic
*Renin acts on zona glomerulosa producing aldosterone
*Increases absorption of Na+ and increased K+ excretion
*Blood volume increases and/or BP

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25
Q

What happens during stress?

A

Stress
*CRH released
*ACTH released
*Drives adrenal gland to release glucocorticoids (ie cortisol)
*Helps body overcome stress

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26
Q

What does FSH and LH stimulate?

A

Hypothalamus -> GnRH -> AP -> FSH/LH -> ovaries/testes.
FSH acts on granulosa cells to produce oestrogen and sertoli cells to stimulate spermatogenesis.
LH acts on theca cells to produce androgens or leydig cells to produce testosterone.

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27
Q

BMI thresholds

A

<18.5 underweight
18.5 - 24.9 normal
25.0 - 29.9 overweight
30.0 - 39.9 obese
>40 morbidly obese

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28
Q

What is obesity a risk factor of?

A
  1. Type II diabetes
  2. Hypertension
  3. Coronary artery disease
  4. Stroke
  5. Osteoarthritis
  6. Obstructive sleep apnoea
  7. Carcinoma
    - Breast
    - Endometrium
    - Prostate
    - Colon
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29
Q

How would you calculate BMI?

A

wt (kg)/ht (m^2)

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30
Q

Give a reason to why working night shifts could increase obesity?

A

Disruption of the Circadian rhythm, this could increase insulin resistance leading to obesity.

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31
Q

What are the two factors that can affect weight regulation?

A
  • Genetics
  • Environment
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32
Q

What are the three main organs that influence appetite regulation?

A
  • GI tract
  • Brain
  • Adipose tissue
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33
Q

Why are the two factors that drive us to eat?

A

Internal physiological drive to eat
- feeling that prompts thought of food and motivates food consumption

External psychological drive to eat
- sometimes even in the absence of hunger (ie buffet)

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34
Q

What are the 4 main stages in the satiety cascade?

A
  1. Sensory
  2. Cognitive
  3. Post ingestive
  4. Post absorptive.
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35
Q

Which brain structure is responsible for appetite regulation?

A

Hypothalamus
Lateral hypothalamus - hunger centre
Ventromedial hypothalamic nucleus - satiety center

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36
Q

Which hormones suppress appetite?

A
  • Leptin
  • Insulin
  • PYY
  • CCK
  • POMC
  • CART
  • GLP 1
  • Serotonin
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37
Q

Which hormones increase appetite?

A
  • Ghrelin
  • NPY
  • MCH
  • AgRP
  • Orexin
  • Endocannabinoid
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38
Q

Where is leptin released from?

A

White adipose tissue

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39
Q

What is the mechanism of action of leptin on the hypothalamus?

A

*Leptin inhibits NPY and AgRP
*Leptin stimulates POMC and CART
*Appetite decreases

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40
Q

What might happen if someone was deficient in leptin?

A

They might become obese.

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41
Q

Where does CCK act on?

A

Stretches receptors on the pyloric sphincter
- Delays gastric emptying
- Gall bladder contraction
- Insulin release

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42
Q

Where is ghrelin expressed?

A

In the stomach

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43
Q

How does ghrelin stimulate appetite?

A

Ghrelin stimulates NPY and AGRP = increases appetite.

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44
Q

Which hormone decreases following gastric bypass surgery?

A

Ghrelin

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45
Q

What hormone might it be possible to use in the treatment of anorexia?

A

Ghrelin

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46
Q

What can POMC be broken down into? What roles do they play?

A

Three main hormones:
- ACTH
- MSH
- endorphin

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47
Q

What can POMC deficiency lead to?

A
  • Pale skin
  • Adrenal insufficiency
  • Hyperphagia and obesity
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48
Q

What does high levels of agouti-related peptide (AgRP) cause?

A

Causes excess eating, increases appetite

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49
Q

What is the role of Malonyl CoA in satiety?

A

In a fasted state, action of different hormones will lead to activation of AMPK

Increased AMPK will reduce acetyl CoA Carboxylase and decrease malonyl CoA and increase appetite.

In a fed state, the opposite occurs.

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50
Q

In non diabetic humans how does metabolism occur during the fasting state?

A

*All glucose comes from liver (and a bit from kidney)
- Breakdown of glycogen
- Gluconeogenesis (utilises 3 carbon precursors to synthesise glucose including lactate, alanine and glycerol)
*Glucose is delivered to insulin independent tissues, brain and red blood cells
*Insulin levels are low
*Muscle uses FFA for fuel
*Some processes are very sensitive to insulin, even low insulin levels prevent unrestrained breakdown of fat

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51
Q

In non diabetic humans how does metabolism occur after feeding ?

A

*Rising glucose (5-10 min after eating) stimulates insulin secretion and suppresses glucagon
*40% of ingested glucose goes to liver and 60% to periphery, mostly muscle
*Ingested glucose helps to replenish glycogen stores both in liver and muscle
*High insulin and glucose levels suppress lipolysis and levels of non-esterified fatty acids (NEFA or FFA) fall

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52
Q

Define diabetes mellitus

A

A disorder of carbohydrate metabolism characterised by hyperglycaemia.

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53
Q

How does diabetes mellitus cause morbidity and mortality?

A

Causes morbidity and mortality through
*Acute hyperglycaemia which if untreated leads to acute metabolic emergencies diabetic ketoacidosis (DKA) and hyperosmolar coma (Hyperosmolar Hyperglycaemic State )
*Chronic hyperglycaemia leading to tissue complications (macrovascular and microvascular)
*Side effects of treatment- hypoglycaemia

54
Q

What types of complications are associated with diabetes?

A

*Diabetic retinopathy
*Diabetic nephropathy
*Stroke
*Cardiovascular disease
*Diabetic neuropathy

55
Q

What are the different types of diabetes?

A

*Type 1
*Type 2
- Includes gestational and medication induced diabetes
*Maturity onset diabetes of youth (MODY), also called monogenic diabetes
*Pancreatic diabetes
*“Endocrine Diabetes” (Acromegaly/Cushings)
*Malnutrition related diabetes

56
Q

Diagnostic criteria for diabetes

A

If symptomatic:

*Random plasma glucose > 11 mmol/l
*Fasting plasma glucose > 7 mmol/l

If asymptomatic:

  • Glucose tolerance test (75g glucose) fasting > 7 or 2h value > 11 mmol/l (repeated on 2 occasions)
    *HbA1c of > 48mmol/mol (6.5%)
57
Q

Pathogenesis of Type 1 diabetes

A
  • no insulin produced -> glucose not transported to cells -> hyperglycaemia
  • Insulin allows the glut4 transporter to transport glucose into the cell
    *Body therefore thinks the patient is not eating
    *Liver increases gluconeogenesis to compensate
58
Q

What cells does Type 1 diabetes mellitus affect?

A

Caused by destruction of beta cells of the islet of Langerhans in the pancreas

59
Q

In Type 1 diabetes what does failure of insulin secretion lead to?

A

*Continued breakdown of liver glycogen
*Unrestrained lipolysis and skeletal muscle breakdown providing gluconeogenic precursors
*Inappropriate increase in hepatic glucose output and suppression of peripheral glucose uptake

60
Q

In Type 1 diabetes what does rising glucose concentrations result in?

A

Rising glucose concentration results in increased urinary glucose losses as renal threshold (10mM) is exceeded

61
Q

In Type 1 diabetes what can failure to treat with insulin lead to?

A

Failure to treat with insulin leads to
*Increase in circulating glucagon (loss of local increases in insulin within the islets leads to removal of inhibition of glucagon release), further increasing glucose
*perceived ‘stress’ leads to increased cortisol and adrenaline
*progressive catabolic state and increasing levels of ketones

62
Q

Aetiology of Type 1 Diabetes

A
  • Younger patients (mostly)
  • Higher association in northern europeans
  • Associated with other autoimmune conditions
  • HLA-DR3-DQ2 and HLA-DR4-DQ8
63
Q

Aetiology of Type 2 Diabetes

A
  • Older age
  • Ethnicity (south Asians and Afro-Caribbean)
  • Associated with obesity, lack of exercise, calorie and alcohol excess
  • No immune disturbance
  • No HLA disturbance but there is a stronger genetic link
  • Polygenic disorder
64
Q

In Type 2 diabetes what does insulin resistance and progressive failure of insulin secretion lead to?

A

*Impaired insulin action leads to
- Reduced muscle and fat uptake after eating
- Failure to suppress lipolysis and high circulating FFAs
- Abnormally high glucose output after a meal
*Even low levels of insulin prevent muscle catabolism and ketogenesis so profound muscle breakdown and gluconeogenesis are restrained and ketone production is rarely excessive

65
Q

How often is HbA1c conducted? Why?

A

Every 3 months, as erythrocytes live for 120 days

66
Q

What is the cut off mmol/mol for diabetes?

A

48 (42 is prediabetes)

67
Q

Types of Insulin

A
  • Rapid: aspart, lisporo, novorapid, glulisine
  • Short: regular insulin
  • Intermediate: NPH (half a day)
  • Long: detemir, lantus, glargine
68
Q

T1DM features

A

*Autoimmune condition (β-cell damage) with genetic component
*Profound insulin deficiency

69
Q

T2DM features

A

Insulin resistance
Impaired insulin secretion and progressive β-cell damage but initially continued insulin secretion
Excessive hepatic glucose output
Increased counter-regulatory hormones including glucagon

70
Q

How would you treat Type 2 Diabetes Mellitus?

A
  1. First line is lifestyle modifications and regular HbA1c appointments
  2. Second line if HbA1c still >48 offer METFORMIN
  3. Add one of these drugs:
    * SGLT-2 inhibitors (preferred)
    * DPP-4 inhibitors
    * Sulfonylurea
  4. Triple drug therapy or start insulin
71
Q

Modern insulin therapy in T1D

A

Separation of basal from bolus insulin to mimic physiology

Pre-meal rapid acting boluses adjusted according to pre-meal glucose and carbohydrate content of food to cover meals

Basal insulin should control blood glucose in between meals and particularly during the night

Basal insulin given as either twice daily insulin levemir (basal analogue or once daily degludec) adjusted to maintain fasting blood glucose between 4–7 mmol/L

72
Q

Advantages and disadvantages of basal insulin in T2DM

A

Advantages:
Simple for the patient, adjusts insulin themselves, based on fasting glucose measurements
Carries on with oral therapy, combination therapy is common
Less risk of hypoglycaemia at night

Disadvantages:
Doesn’t cover meals
Best used with long-acting insulin analogues which are considered expensive.

73
Q

Advantages and disadvantages of pre-mixed insulin

A

Advantages:
Both basal and prandial components in a single insulin preparation
Can cover insulin requirements through most of the day

Disadvantages
- Requires consistent meal and exercise pattern
- Cannot seperately titrate individual insulin components
- Increased risk of nocturnal and fasting hypoglycaemia

74
Q

What is the main factor preventing patients achieving tight glucose targets during treatment?

A

Hypoglycaemia

75
Q

Why does hypoglycaemia occur in patients undergoing insulin therapy?

A

Hypoglycaemia occurs due to the inability of insulin therapy to mimic the physiology of the beta cell

76
Q

How do you classify hypoglycaemia

A

Level 1:
Alert value
Plasma glucose <3.9 mmol/l (70 mg/dl) and no symptoms

Level 2:
Serious biochemical
Plasma glucose <3.0 mmol/l
(55 mg/dl)

Level 3:
Patient has impaired cognitive function sufficient to require external help to recover

77
Q

Non-severe versus severe symptomatic hypoglycaemia

A

Non-severe: Patient has symptoms but can self-treat and cognitive function is mildly impaired
Severe: Patient has impaired cognitive function sufficient to require external help to recover

78
Q

What pathophysiological effects does hypoglycaemia have on different organs and systems?

A

Brain:
Cognitive dysfunction
Blackouts, seizures, comas
Psychological effects

79
Q

Common hypoglycaemia symptoms
(include the autonomic, neuroglycopenic and non-specific symptoms)

A
  1. Development of symptoms
    Autonomic:
    - Trembling, palpitations, sweating, anxiety, hunger
    Neuroglycopenic:
    - difficulty concentrating, confusion, weakness, drowsiness, vision changes, difficulty speaking
    Non-specific:
    - nausea, headache
  2. Low blood glucose (<3.9 mmol/l)*
  3. Response to treatment with carbohydrate
80
Q

Causes of hypoglycaemia

A

*Use of drugs (prescribed, alcohol)
*Increasing age
*Increased physical activity
*Long duration of diabetes
*Tight glycaemic control with repeated episodes of non severe hypoglycaemia
*Sleeping

81
Q

Screening for risk of severe hypoglycaemia

A

Screening should be based on established risk factors
*Low HbA1c; high pre-treatment HbA1c in T2DM
*Long duration of diabetes
*A history of previous hypoglycaemia
Impaired awareness of hypoglycaemia (IAH)
*Recent episodes of severe hypoglycaemia
*Daily insulin dosage >0.85 U/kg/day
*Physically active (e.g. athlete)
*Impaired renal and/or liver function

82
Q

Strategies to prevent hypoglycaemia

A

*Patient education
*Consider enrolling patients with frequent hypoglycaemia in a blood glucose awareness training programme

83
Q

How would you treat hypoglycaemia?

A

Recognize symptoms so they can be treated as soon as they occur

Confirm the need for treatment if possible (blood glucose <3.9 mmol/l is the alert value)

Treat with 15 g fast-acting carbohydrate to relieve symptoms

Retest in 15 minutes to ensure blood glucose >4.0 mmol/l and re-treat (see above) if needed

Eat a long-acting carbohydrate to prevent recurrence of symptoms

84
Q

What are the actions of PTH?

A

Acts on the kidney to
*increase Ca2+ reabsorption
*decrease phosphate reabsorption.
*1 α - hydroxylation of 25-OH vit D

Increases bone remodelling
Bone resorption > Bone formation

85
Q

PTH response to decreased serum calcium

A

*Increase bone resorption
*Increase Ca2+ absorption
*Increase Ca2+ reabsorption

86
Q

A person with low serum albumin might have low total serum calcium but not a low ionised calcium. What is the corrected calcium if:
serum calcium = 2.08 mmol/L
serum albumin = 30 g/L

A

corrected calcium = total serum calcium + 0.02 * (40 – serum albumin)

2.08 + 0.02 * (40 - 30)
= 2.28 mmol/L

87
Q

Consequences of Hypocalcaemia

A

*Parasthesia
*Muscle spasm
o Hands and feet
o Larynx
o Premature labour
*Seizures
*Basal ganglia calcification
*Cataracts
*ECG abnormalities
o Long QT interva

88
Q

What two signs can be used as a physical test for hypocalcaemia?

A
  • Chvostek sign
    Tap over the facial nerve
    Look for spasm of facial muscle
  • Trousseau sign
    Inflate the blood pressure cuff
    to 20 mm Hg above systolic
    for 5 minutes
89
Q

Cause of hypocalcemia?

A

Vitamin D deficiency

90
Q

Causes of hypoparathyroidism?

A
  • Syndromes
  • Di George syndrome
  • Genetic
  • Surgical
  • Radiation
  • Autoimmune
  • Infiltration
  • Magnesium deficiency
91
Q

What leads to pseudohypoparathyroidism?

A

Resistance to parathyroid hormone
- Usually Type 1 Albright hereditary osteodystrophy - caused by mutation with deficient Gα subunit

92
Q

Pseudohypoparathyroidism symptoms

A

*Short stature
* Obesity
* Round facies
* Mild learning difficulties
* Subcutaneous ossification
* Short fourth metacarpals
* Other hormone resistance

93
Q

Common reasons for misdiagnosis of hypercalcemia

A
  • Tourniquet on for too long
  • Sample old and haemolysed
94
Q

Hypercalcaemia: Symptoms and Consequences

A
  • Thirst, polyuria
  • Nausea
  • Constipation
  • Confusion coma
  • Renal stones
  • ECG abnormalities - Short QT
95
Q

Causes of hypercalcaemia

A

90% is due to
*Malignancy: bone met, myeloma, lymphoma
*Primary hyperparathyroidism

Other causes:
*Thiazides
* Thyrotoxocosis
* Sarcoidosis
* Familial hypocalciuric / benign hypercalcaemia
* Immobilisation
* Milk-alkali
* Adrenal insufficiency
* Phaeochromocytoma

96
Q

Primary Hyperparathyroidism consequences

A

*Bones
o Osteitis fibrosa cystica
o Osteoporosis
* Kidney stones
* Psychic groans
o confusion
* Abdominal moans
o Constipation
o Acute pancreatitis

97
Q

What is hyperparathyroidism usually caused by?

A

80% due to single benign adenoma
15-20% due to four gland hyperplasia
<0.5% malignant

98
Q

What does excess cortisol lead to?

A

Cushing’s syndrome

99
Q

What does Cushing’s syndrome lead to?

A
  • Central obesity
  • Proximal muscle wasting
  • Hirsutism (females grow male facial hair)
  • Easy bruising
100
Q

What leads to excess cortisol being released - leading to Cushing’s syndrome?

A

Most commonly caused by pituitary adenoma

101
Q

Health consequences of Cushing’s syndrome?

A

Metabolic - HTN, T2DM, Dyslipidaemia, osteoporosis
Mental - anxiety, depression, insomnia

102
Q

How would you diagnose Cushing’s syndrome? Describe briefly how it works

A

Dexamethasone suppression tests

Dexamethasone given -> negative feedback on hypothalamus -> reduced CRH -> reduced ACTH from pituitary -> low cortisol

No cortisol suppression -> suggests Cushing’s syndrome

103
Q

Common cause of Graves disease?

A

Most common - Graves disease
Also common - De Quervain’s or acute thyroiditis

104
Q

Complication of Graves disease

A

Thyroid storm

105
Q

Common cause of hypothyroidism?

A

Hashimoto’s

106
Q

What deficiency is the most common cause of hypothyroidism in developing countries?

A

Iodine deficiency

107
Q

What iatrogenic reasons may lead to hypothyroidism?

A

Treatments for hyperthyroidism such as lithium and amiodarone

108
Q

Hypothyroidism symptoms?

A
  • Dry skin and hair, brittle nails, lateral loss of eyebrows
  • Fatigue and weakness
  • Weight gain and fluid retention
  • Cold sensitivity
  • Constipation
  • Heavy or irregular periods
109
Q

Hyperthyroidism symptoms?

A
  • Nervousness, anxiety, irritability
  • Increased heart rate/ palpitations
  • Weight loss and increased appetite
  • Heat intolerance and sweating
  • Oligomenorrhea
110
Q

True or False:
Thyroxine is the active form of triiodothyronine?

A

False
Thyroxine - T4
Triiodothyronine - T3

T3 is the active form of T4

111
Q

What is Graves’ disease?

A

Thyroid stimulating hormone receptor antibodies stimulate the thyroid gland, leading to overproduction of thyroid T3/T4

112
Q

Symptoms of Graves’ disease

A
  • Weight loss
  • Increased heart rate
  • Painless Goitre and Pathognomonic
  • Exophthalmos
  • Pretibial myxedema
  • Thyroid acropachy
113
Q

Graves’ disease treatment?

A

Medical treatment is block (using Carbimazole and Propylthiouracil) and replace (using levothyroxine)

Carbimazole is contraindicated in pregnant women as it’s teratogenic. Should use propylthiouracil.

  • Reduction of thyroid gland surgically with thyroidectomy or radioiodine (Short/life, thyroid-specific)
114
Q

What is De Quervain’s thyroiditis caused by?

A

It is an inflammatory condition typically triggered by a viral infection - flu like symptoms are present. This causes the release of stored thyroid hormones (hyperthyroidism).

115
Q

Hashimoto’s cause?

A

Autoimmune disorder causing anti-thyroid antibodies to damage the thyroid. Decreasing production of T4/T3
Investigations show increased TSH with T3/T4. 90% will have TPO antibodies

116
Q

Treatment of Hashimoto’s

A

Levothyroxine

117
Q

A 14 year old boy presents to your GP clinic with his mother. The patient is complaining of feeling tired and going to the toilet frequently. He mentioned that he always need to keep drinking because he’s so thirsty all the time. His general appearance is quite slim. His PMhx is not significant but his mother mentioned that she suffers from hypothyroidism. What is the likely diagnosis?

a) Hashimoto’s
b) Graves’ disease
c) Type 1 diabetes meticullus
d) Type 2 diabetes meticullus
e) Diabetes insipidus

A

c) Type 1 diabetes meticullus

118
Q

A 14 year old boy presents to the emergency department with his mother. He has been vomiting, looks drowsy and generally unwell. He is breathing very rapidly and you note that his breath smells fruity. On examination his skin has reduced turgor, his blood pressure is 90/50 and HR 135. What is the likely diagnosis?

A

Diabetic ketoacidosis

119
Q

What is diabetic ketoacidosis?

A

It is metabolic acidosis caused by untreated type 1 diabetes (occasionally type 2) or undiagnosed diabetes

120
Q

DKA diagnostic criteria

A

Glucose >11 mmol/l
pH < 7.3
Bicarbonate <15 mmol/l
Ketones >3 mmol/l

121
Q

Pathophysiology of diabetic ketoacidosis?

A

Complete lack of insulin causes uncontrolled lipolysis. Breakdown of fats -> increased fatty acids -> converted to ketones -> metabolic acidosis

122
Q

DKA management?

A

FIG PICK

F - fluids first
I - Insulin
G - glucose
P - potassium
I - infection
C - chart fluid balance
K - ketone monitoring

123
Q

Main complication of DKA management?

A

Cerebral oedema - caused by rapid fluid replacement

124
Q

You have given fluids to a patient with DKA what is the next step?

A

Insulin with dextrose

125
Q

What serum ketones is needed to diagnose DKA?

A

> 3 mmol

126
Q

A 44 year old man presents to your GP clinic. He is complaining of always needing to urinate and increased thirst. He has a BMI of 30 and has noted that he is losing feeling in his toes. What is the likely diagnosis?

A

Type 2 diabetes mellitus

127
Q

What is hyperosmolar hyperglycaemic state?

A

Medical emergency due to chronic T2DM. Severe hyperglycemia over time will cause
*severe osmotic diuresis
*severe dehydration
*electrolyte deficiency

128
Q

Diagnosis of hyperosmolar hyperglycaemic state?

A

No specific criteria
*Hyperglycaemia > 30 mmol
*Serum Osmolarity > 320 mosmol/kg
*No ketonemia

129
Q

Pathophysiology of diabetes insipidus?

A

Insufficient ADH secreted from posterior pituitary. Causes can be nephrogenic or neurogenic.

Nephrogenic - pathology of kidneys - unable to respond to ADH

Neurogenic - reduced ADH - excessive water loss

130
Q

How would you diagnose diabetes insipidus

A

Water deprivation test and ADH suppression

131
Q

Management of diabetes insipidus

A

Neurogenic
- desmopressin: increased water reabsorption

Nephrogenic
- Diuretics

132
Q

What is the definitive treatment of Conn’s syndrome?

A

Adrenalectomy

2A (7 decks)

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