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phase 2 medicine > Endocrine system > Flashcards

Endocrine system Flashcards

1
Q

what are the components of the endocrine system

A

pituitary, thyroid, parathyroid, adrenal glands, pancreas, ovary/testes

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1
Q

endocrine vs exocrine glands

A

endocrine –> secretions into blood

exocrine –> secretion into ducts

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2
Q

what are paracrine and autocrine actions

A

paracrine –> acts on adjacent cells
autocrine –> acts on cell which secreted hormone

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3
Q

water soluble hormones vs fat soluble hormones

A

water soluble
- travels unbound
- binds to surface receptor of interactions
- short half life
- fast clearance

fat-soluble
- travels by protein binding
- diffuses into cell for interactions
- long half life
- slow clearance

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4
Q

give an example of a peptide hormone

A

insulin, LH, FSH

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5
Q

what are characteristics of peptide hormones (polarity, storage and release)

A

hydrophilic
stored in secretory granules
released in pulses or bursts

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6
Q

what is proinsulin made of

A

C-peptide and insulin joined by cystine bonds

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7
Q

How does the insulin receptor work

A

binding of insulin to the alpha domain leads to phosphorylation of tyrosine kinase and leads to cascade reactions which drive glucose uptake

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8
Q

what type of hormone is dopamine

A

amine

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9
Q

what do you call thyroid hormones

A

iodothyronines

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10
Q

how is thyroid hormone synthesised and released

A

SYNTHESIS
thyroid follicular cells secrete thyroglobulin into colloid

iodine gets incorporated in thyroglobulin –> iodothyrosines

conjugation of iodotyrosines gives rise to T3 and T4

RELEASE
hypothalamus produces thyrotropin releasing hormone

this causes pituitary to release thyroid stimulating hormone

TSH binds to TSHR (receptor) and stimulates movement of colloid into follicular cell where T4 and T3 get cleaved from thyroglobulin

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11
Q

which is the active form? iodide or iodine

A

iodine

iodide –> dide for DEAD

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12
Q

how do nuclear receptor hormones work? give examples

A

they directly bind to DNA and affect transcription –> they function as transcription factors

Oestrogen, Thyroid Hormone, Vitamin D

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13
Q

what transports Vit D and How does it function as a hormone

A

it is transported by Vit D binding protein

it enters the cell directly in the nucleus to stimulate more absorption of calicum and phosphate

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14
Q

how do steroid hormones act?

A

diffuse through plasma membrane (hydrophobic)
bind to receptor
receptor hormone complex enters nucleus and binds to GRE
binding to a DNA region promotes transcription of that gene to mRNA

mRNA leads to protein synthesis

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15
Q

which hormones have a circadian rhythm

A

cortisol
prolactin
GH
LH
FSH
melatonin

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16
Q

what hormones are secreted by the posterior pituitary

A

oxytocin and ADH

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17
Q

what are the functions of oxytocin

A

lactation and uterus/cervical dilation

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18
Q

if a patient has abnormal hormonal tests what is the next test you would perform

A

MRI of pituitary

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19
Q

what are the functions of growth hormone

A

growth promotion and metabolism

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20
Q

what effect does growth hormone have on insulin and why

A

inhibiting –> promotes fat and carbohydrate metabolism

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21
Q

what effect does GH have on blood glucose

A

increase blood glucose

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22
Q

what effect does GH have on the liver and other tissues

A

Production of IGFs (insulin like growth factors)

leads to cell proliferation and cell growth

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23
Q

draw the HPT axis

A

hypothalamus > TRH . ant pituitary > TSH > Thyroid gland > Thyroid hormones > Target cells

negative feedback loops:
TSH inhibits hypothalamus and Thyroid hormones inhibit the ant pituitary and the hypothalamus

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24
Q

what is the blood supply of the thyroid

A

Inferior thyroid artery from the subclavian thyrocervical trunk
Superior thyroid artery from the external carotid

In some people there is also the IMA artery from the brachiocephalic trunk

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25
Q

what are the functions of the thyroid hormone

A

Accelerates food metabolism
Increases protein synthesis
Stimulation of carbohydrate and fat metabolism
Increase in ventilation rate, CO and HR
Brain development during foetal life and postnatal development
Growth rate accelerated

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26
Q

draw the HPA axis

A

hypothalamus > CRH > Ant pituitary > ACTH > Adrenal cortex > cortisol

Negative feedback loop:
Cortisol inhibits both the Ant pituitary and the Hypothalamus

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27
Q

functions of cortisol

A

increase metabolism of glucose (diabetes! - cortisol increases blood sugar)
control your blood pressure
reduce inflammation

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28
Q

what are the layers of the adrenal gland

A

capsule
zona glomerulosa
zona fasciulata
zona reticularis
adrenal medulla

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29
Q

what do the specific areas of the adrenals secrete

A

CORTEX
Zona glomerulosa (mineralocorticoids)
aldosterone

Zona fasciculata (glucocorticoids)
cortisol

Zona reticulata (androgens)
adrostenedione
DHEA

MEDULLA (catecholamines)
Epinephrine and Norepinephrine

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30
Q

what is the short term vs the long term response to stress in terms of hormone secretion

A

short-term –> epinephrine and norepinephrine (catecholamines)
long-term –> mineralocorticoids and glucocorticoids (aldosterone and cortisol)

all of these lead to increased blood glucose, immune suppression and increase in blood volume and blood pressure

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31
Q

what is the hormone produced by the heart and what does it do

A

ANP
decreases BP by promoting Na and H2O excretion
VASODILATION
also dilates afferent arteriole to increase GFR

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32
Q

where is IGF-I synthesised

A

Liver

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33
Q

where is erythropoietin synthesised

A

kidney

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34
Q

what hormones do blood vessels secrete

A

endothelin
NO
prostaglandins

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35
Q

what is the BMI formula

A

wt (kg)/ht (m2)

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36
Q

what are the BMI ranges

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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37
Q

what are the risks of obesity

A

Type II diabetes
Hypertension
Coronary artery disease
Stroke
Osteoarthritis
Obstructive sleep apnoea
Carcinoma
- Breast
- Endometrium
- Prostate
- Colon

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38
Q

what parts of the brain play a role in appetite regulation and what exactly do they control

A

lateral hypothalamus –> hunger
ventromedial hypothalamic nucleus –> satiety centre

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39
Q

what things control appetite

A

psychological factors
cultural factors
neural afferents –> vagus
Hormones like leptin insulin and cortisol
glucose and ketones
CCK
Ghrelin

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40
Q

where is leptin secreted from and what is its function

A

white adipose tissue
Switches off appetite and is
immunostimulatory

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41
Q

what is the function of peptide YY, what is it secreted by, and on what receptors does it act

A

binds to NPY receptors and secreted in response to food to inhibit gastric motility and appetite
secreted by neuroendocrine cells in the ileum pancreas and colon

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42
Q

what is the function of CCK and where are its receptors

A

receptors: pyloric sphincter
function:
- delays gastric emptying
- contracts gall bladder
- stimulates insulin release

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43
Q

draw the cycle of neurohormonal regulation of eating

A

look at appetite regulation slides

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44
Q

where is ghrelin expressed and what is its function

A

expressed in stomach and stimulates GH release and increases appetite

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45
Q

what are the functions of incretins

A

Reduce glucagon only when blood sugar is NORMAL OR HIGH, not when it’s low.
Boost insulin production only when blood sugar is HIGH, avoiding drops in blood sugar.
They improve the feeling of fullness after eating, aiding in appetite control.
They slow down the movement of food from the stomach to the intestine, helping control blood sugar spikes after meals.

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46
Q

what is the site of insulin and glucagon secretion

A

islet of langerhans

Beta cells - insulin
alpha cells - glucagon

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47
Q

what cells secrete somatostatin and PP (pancreatic polypeptide)

A

All cells are in the Islets of langerhans
Delta cells - somatostatin
F cells - Pancreatic polypeptide

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48
Q

explain the metabolism of carbohydrates in the fasting state

A

you get glucose via breakdown of glycogen and gluconeogenisis
glucose is used by important things like rbc and brain
insulin levels are low
muscles use free fatty acids for fuel

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49
Q

what is the relationship between alpha and beta cells in the islets of langerhans

A

they are glucagon and insulin secreting respectively and they are right next to each other so that they can have paracrine crosstalk and inhibit each other

ex.: local insulin release will inhibit glucagon release

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50
Q

explain the insulin secretion by the beta cell

A

1) glucose enters beta cell via GLUT 2 transporter
2) glucose metabolism forms ATP which leads to a conformational change in the Kir6.2 channel –> channel closes
3) Kir6.2 normally allows K+ diffusion in the cell so when the channel is closed the beta cell becomes depolarised which allows Ca+2 channels to open
4) opening of Ca+2 channels triggers insulin vesicle exocytosis

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51
Q

how does insulin act on muscle and fat cells

A

activation of insulin receptors triggers mobilisation of vesicles with GLUT4 channel prot to the plasma membrane –> more channel prot allows for more “doors” for glucose entry in the cell –> accelerates diffusion of glucose into cell

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52
Q

what are the functions of insulin

A

Supresses hepatic glucose output
decreases Glycogenolysis
decreases Gluconeogenesis
Increases glucose uptake into insulin sensitive tissues (muscle, fat)
supress Lipolysis
surpress Breakdown of muscle

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53
Q

what are the functions of glucagon

A

Increases hepatic glucose output
increases Glycogenolysis
increases Gluconeogenesis
Reduces glucose uptake into tissues (cuz you want more in blood)
Stimulate peripheral release of gluconeogenic precursors (glycerol, AAs)
Lipolysis
Muscle glycogenolysis and breakdown

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54
Q

what are the consequences of acute and chronic hyperglycaemia in diabetes mellitus

A

Acute hyperglycaemia which if untreated leads to acute metabolic emergencies:
- diabetic ketoacidosis (DKA)
- hyperosmolar coma (Hyperosmolar Hyperglycaemic State )

Chronic hyperglycaemia leading to tissue complications (macrovascular and microvascular) neuropathies, nephropathies, retinopathies

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55
Q

what are possible complications of diabetes

A

diabetic retinopathy –> vision loss
diabetic nephropathy –> Kidney failure
stroke
CVD
Diabetic Neuropathy –> loss of sensation in extremities; amputations

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56
Q

what is the most common cause of death and disability in diabetics

A

CVD

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57
Q

what are the 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

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58
Q

what are the blood tests for diabetes and what values indicate diabetes

A

Random plasma glucose > 11 mmol/l

Fasting plasma glucose > 7 mmol/l

GTT (Glucose Tolerance Test) - after fasting glucose test you give patient a drink of glucose solution - after 2h measure value > 11 mmol/l (repeated on 2 occasions)

HbA1c (glycated hemoglobin- is a measure of average blood sugar levels over the past 2-3 months) of > 48mmol/mol (6.5%)

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59
Q

what is the pathophysiology of type 1 diabetes

A

loss of beta cells due to autoimmune destruction leads to insulin deficiency

autoimmune response is because beta cells express HLA antigens which results in chronic cell mediated immune response –> chronic insulitis

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60
Q

what are the results of insufficient insulin secretion

A

Uncontrolled breakdown of glycogen from liver, fats and muscles, providing materials for glucose production.
Liver produces more glucose while peripheral uptake decreases.
High glucose levels prompt excess glucose loss in urine (exceeding renal threshold).

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61
Q

what does failure of insulin treatment in type 1 diabetes lead to

A

Increased circulating glucagon due to reduced local insulin effects.
Stress responses trigger elevated cortisol and adrenaline levels.
Progression into a catabolic state with rising ketone levels.

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62
Q

what is IGT

A

IGT stands for Impaired Glucose Tolerance, which is a condition where blood sugar levels are higher than normal but not high enough to be classified as diabetes. It’s often considered a pre-diabetic state.

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63
Q

why does type 1 diabetes result in ketoacidosis and type 2 diabetes is much less likely to

A

Ketone Production in Type 1 Diabetes:
Insulin shortage due to immune attack on pancreatic beta cells.
Glucose can’t be effectively used for energy without sufficient insulin.
Body compensates by breaking down fats for energy.
Result: Ketone production (acetoacetate, beta-hydroxybutyrate, acetone).

Difference in Type 2 Diabetes:
Type 2 involves insulin resistance but still has insulin production; even a little bit of insulin help to prevent ketogenisis

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63
Q

type 1 vs type 2 diabetes

A

type 1 is characterised by absent insulin production

type 2 is characterised by insulin RESISTANCE and progressive failure of insulin secretion

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64
Q

what causes the insulin resistance in type 2 diabetes

A

Genetic predisposition
Environmental factors (obesity and lack of physical activity)
Lipid deposition in liver and pancreas lead to both insulin resistance and impaired insulin secretion

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65
Q

how do you treat type 2 diabetes

A

weight loss and exercise which if substantial can reverse hyperglycaemia

BP medication and blood glucose and lipids medications

metmorphin –> Reduce gluconeogenesis in liver (gluconeogenesis increased in T2DM due to excess glucagon)

sulphonylureas –> medications which stimulate insulin release and improve glycaemic control but at the expense of weight gain

Glitazone (aka thiazolidinediones) –> Enhance uptake of fatty acids & glucose by improving insulin sensitivity but increase weight, risk of heart failure, and risk of fractures

DPP4 Inhibitors - prolong effect of GLP-1

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66
Q

what is GLP-1, who is it secreted by and what is its function

A

glucagon-like peptide
it is an incretin
secreted by L cells in intestine
stimulates insulin secretion and
suppresses glucagon
slows gastric emptying
reduces appetite
improves insulin sensitivity

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67
Q

what is basal bolus therapy

A

it is a diabetes therapy which uses two types of insulin: basal insulin and bolus insulin

basal insulin provides a constant background insulin level which helps control blood sugar levels between meals

bolus insulin is fast acting and it is usually taken after meals to handle the rapid surge in blood glucose

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68
Q

how are basal bolus insulin levels throughout the day different to insulin levels in a normal person

A

slow increase in insulin levels after subcutaneous injections and slower decline in insulin levels following meals

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69
Q

what are the advantages and disadvantages of basal insulin in type 2 diabetes

A

advantages
Simple for the patient, adjusts insulin themselves based on fasting glucose measurements (personalization of dose)
Carries on with oral therapy, combination therapy is common
Less risk of hypoglycemia at night

disadvantages
Doesn’t cover rise in blood sugar after meals
Best used with long-acting insulin analogues which are considered expensive.

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69
Q

advantages and disadvantages of pre-mixed insulin in diabetes

A

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

Disadvantages
- Not physiological
- Requires consistent meal and exercise pattern
- Comes as a fixed mix –> can’t change dose of different components
- increased risk for nocturnal hypoglycaemia
- increased risk for fasting hyperglycaemia if basal component does not last long enough
- Often requires accepting higher HbA1c goal of <7.5% or ≤8% (<58 or ≤64 mmol/mol)2,3

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70
Q

what are the differences between T1DM and T2DM treatment

A

Oral medications are not typically part of the treatment regimen for type 1 diabetes. Basal-bolus therapy is used.
Oral medications are often a first-line treatment for type 2 diabetes. Basal -bolus only used as disease progresses.

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71
Q

what is the difference between severe and non-severe hypoglycaemia

A

severe - Patient has impaired cognitive function sufficient to require external help to recover; plasma glucose in less than 3 mmol/l

non-severe - Patient has symptoms but can self-treat and cognitive function is mildly impaired; plasma glucose is less than 3.9 mmol/l

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72
Q

what are complications of hypoglycaemia

A

Brain - cognitive disfunction - seizures, comas

Heart - increased risk of miocardial ischemia and cardiac arrhythmias

Circulation - endothelial dysfunction and inflammation; blood coag abnormalities

Muscle Weakness - Due to decreased energy supply, interruption of nerve signalling, and release of adrenalin

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73
Q

common symptoms of hypoglycaemia

A

AUTONOMIC:
Trembling
Palpitations
Sweating
Anxiety
Hunger

NEUROGLYCOPENIC:
Difficulty concentrating
Confusion
Weakness
Drowsiness, dizziness
Vision changes
Difficulty speaking

NON-SPECIFIC:
Nausea
Headache

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74
Q

what are the physiological responses to preventing hyperglycaemia

A

Inhibition of endogenous insulin secretion
Secretion of glucagon and adrenaline

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75
Q

what are the causes of hypoglycaemia?

A

Long duration of diabetes

Tight glycaemic control with repeated episodes of non-severe hypoglycaemia

Increasing age

Increased physical activity

Sleeping

Use of drugs and alcohol

Not eating

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76
Q

how do you treat hypoglycaemia?

A

15 g fast-acting carbohydrate to relieve symptoms
retest blood in 15 minutes to ensure blood glucose levels > 4.0 mmol/L
Eat a long-acting carbohydrate to prevent recurrence of symptoms

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76
Q

why does hypoglycaemia happen to diabetics from a physiological perspective?

A

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

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77
Q

what are the functions of the parathyroid hormone?

A

increased gut Ca+2 ABSORPTION and renal Ca+2 REabsorption
phosphate excretion
increased Vit D3 levels for increased Ca+2 absorption
Decrease FGF-23
increased bone RESORPTION

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78
Q

what is the response of PTH to decreased serum calcium?

A

increase in PTH secretion to enhance Ca+2 absorption via gut, reabsorption via the renal system, and resorption from bone stores.

Vit D synthesis also increases to aid intestinal absorption of Ca+2

Phosphate excretion increases because phosphate and calcium are tightly coupled in bone tissue. When PTH stimulates bone resorption, calcium and phosphate are uncoupled and released into the bloodstream. The PTH will increase Ca+2 reabsorption and decrease PO4-3 reabsorption.

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79
Q

why is calcium homeostasis important?

A

functioning of muscles and nerves (heart muscle, skeletal muscle, and nerve impulses depend on calcium movement)

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80
Q

why do you have to be careful with serum calcium readings?

A

because the serum calcium reading includes both free-floating ionised calcium which is active and the calcium which is albumin-bound. If you have a low serum calcium reading it might actually just be due to hypoalbuminemia, not necessarily low active calcium levels in the blood. Your active calcium levels might still be normal.

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81
Q

what are the consequences of hypocalcaemia?

A

paresthesia
muscle spasm
seizures
basal ganglia calcification
cataracts
ECG abnormalities
long QT intervals

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82
Q

what is Chvostek’s sign and how is it tested

A

A positive Chvostek’s sign, which is characterized by facial twitching in response to tapping the facial nerve in front of the ear, can be indicative of hypocalcemia in some cases.

This sign is one of the clinical manifestations of hypocalcemia, suggesting increased neuromuscular irritability due to low blood calcium levels. When the facial nerve is tapped in individuals with hypocalcemia, it can trigger involuntary muscle contractions or twitching in the facial muscles.

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83
Q

what is Trousseau’s sign and how is it tested

A

Trousseau’s sign is a clinical sign used in medicine to indicate increased neuromuscular irritability associated with hypocalcemia

The sign is elicited by inflating a blood pressure cuff on the arm to a pressure higher than the systolic blood pressure for a few minutes. This occlusion of blood flow can result in ischemia to the tissues below the cuff. In individuals with hypocalcemia, this brief ischemic episode can trigger involuntary muscle twitching or spasms which might cause flexion of the wrist, thumb and metacarpophalangeal joints, resulting in a characteristic hand posture resembling a claw or “paddle-shaped” hand.

*there is no flexion of the interphalangeal joints

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84
Q

what are the possible causes of hypocalcaemia?

A

vit d deficiency
hypoparathyroidism
pseudohypoparathyroidism

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85
Q

what are the causes of hypoparathyroidism?

A

surgical
radiation
Di George syndrome –> developmental abnormality which leads to many congenital defects
Genetic cause
Autoimmune
Magnesium deficiency
very rare but could also be due to hemochromatosis and Wilson’s disease cuz they are characterised by increased iron and copper depositions respectively which could affect the parathyroid gland

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86
Q

what is pseudohypoparathyroidism

A

resistance to PTH

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87
Q

why might keeping the tourniquet on for too long ruin the blood results

A

Prolonged use of a tourniquet during blood collection can cause hemoconcentration due to restricted blood flow. This can lead to an increase in blood components like proteins and electrolytes, affecting certain blood test results. Additionally, hemoconcentration from restricted blood flow might trigger muscle breakdown, releasing substances like calcium, potassium, myoglobin, and creatine kinase into the bloodstream, and potentially altering blood test values.

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88
Q

what are the complications of hypercalcaemia?

A

thirst
polyuria
nausea
constipation
confusion -> coma
renal stones
ECG abnormalities
short QT interval

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89
Q

what are the causes of hypercalcaemia?

A

90% of cases are due to:
Primary hyperparathyroidism
OR
Malignancy - causes unregulated bone breakdown leading to increased calcium levels in the blood
Non-Hodgkin’s Lymphoma
Myeloma
Bone metastases and production of local factors that mobilise calcium
PTHrP – Parathyroid Hormone relating peptide, occurs in some kidney and lung cancers, behaves similarly to PTH but isn’t measured on assay

adrenal insufficiency can also be a cause

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90
Q

what are the consequences of primary hyperparathyroidism?

A

bones, stones, groans, moans

Bones - osteitis fibrosa cystica and osteoporosis

Stones - kidney stones

Psychiatric groans - confusion

Abdominal moans - Nausea, Vomiting, Constipation, Indigestion

also possible cardiac arrest

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91
Q

what are the causes of primary hyperparathyroidism?

A

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

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92
Q

what is the difference between hypoparathyroidism vs pseudohypoparathyroidism?

A

Hypoparathyroidism = insufficient production or secretion of PTH

Pseudohypoparathyroidism = rare genetic disorder where the body exhibits resistance to the action of PTH

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93
Q

what are the 3 vital concepts about pituitary tumours?

A
  1. Pressure on local structures
    e.g. optic nerves – Bitemporal hemianopia
  2. Pressure on normal pituitary – hypopituitarism
  3. Functioning tumour
    – Prolactinoma
    – Acromegaly
    – Cushing’s disease
93
Q

which are the possible diseases of the pituitary

A
  • Benign pituitary adenoma
  • Craniopharygioma
  • Trauma
  • Apoplexy / Sheehans
  • Sarcoid / TB
93
Q

what are possible consequences of pressure on local structures by pituitary tumours

A

can cause:
- headaches —> stretching of dura by tumour
- hydrocephalus (rare)
- visual field defects
- CSF rhinorrhea —> can occur when pituitary tumors extend beyond the sella turcica and erode into adjacent structures, including the sphenoid sinus. Tumors in this region can cause a breakdown in the barrier between the brain and the nasal passages, leading to CSF leakage into the nose.

94
Q

what test can you do to see if there is visual impairment from a pituitary tumour

A

measure visual fields with a red pin

95
Q

what is a prolactin micro adenoma and what does it lead to

A

pituitary tumour which is prolactin-producing and leads to galactorrhoea

96
Q

what are the symptoms of prolactinomas?

A

galactorrhoea
amenorrhoea
infertility
loss of libido/erectile dysfunction
headache
visual field defects (bi-temporal hemianopia)
CSF leak (rare)

97
Q

how do you treat prolactinomas?

A

dopamine agonist: Cabergoline or bromocriptine

98
Q

define puberty

A

physiological, morphological, and behavioural changes as the gonads switch from infantile to adult forms.

99
Q

does a boy’s first ejaculation signify fertility?

A

no

100
Q

what are secondary sexual characteristics

A

Girls:
* Ovarian oestrogens regulate the growth of breast and female genitalia
* Ovarian and adrenal androgens control pubic and axillary hair

Boys:
* Testicular androgens
–External genitalia and pubic hair growth
–enlargement of larynx and laryngeal muscles for voice deepening

101
Q

what tool measures the testicular volume

A

orchidometer

102
Q

what are the functions of oestrogen in female puberty

A

breast growth
labia majora and minora increase in size and thickness
change in colour of outer labia
thickening of hymen
enlargement of clitoris
vestibular glands begin secretion

103
Q

what do pelvic ultrasounds look at in women?

A

Mullerian structures
ovaries morphology
uterus morphology

104
Q

what are adrenal and ovarian androgens responsible for in female puberty?

A

Growth of pubic & axillary hair

105
Q

what is the adrenal androgen

A

DHEA

106
Q

what is precocious puberty?

A

onset of secondary sexual characteristics before 8 yrs (girl), 9 yrs (boy)

107
Q

what is delayed puberty

A

absence of secondary sexual
characteristics by 14 yrs (girl), 16 yrs (boy)

108
Q

what are the consequences of delayed puberty

A

reduced peak bone mass and osteoporosis

109
Q

what are the consequences of menarche before 9 years of age?

A

may lead to short stature

110
Q

draw the female and male HPG axis

A

hypothalamus > GnRH > anterior pituitary > FSH and LH > testes (FSH on sertoli cells and LH on leydig cells)/ovaries (FSH on granulosa cells and LH on theca interna cells) > testosterone/oestradiol/inhibin

negative feedback loops from all products to the pituitary and hypothalamus.

111
Q

what is adrenarche and when does it take place

A

Maturational process of the adrenal gland; specifically the zona reticularis
before puberty

112
Q

what regulates GnRH secretion

A

Increased stimulatory factors most prominently: glutamate and kisspeptin

113
Q

what are the consequences of premature adrenarche?

A

Mild advanced bone age, axillary hair, oily skin, mild acne, body odour

114
Q

what is pubarche

A

Most pronounced clinical result of adrenarche
Pubarche refers to the onset of the development of pubic hair in children as they enter puberty.

115
Q

in what sex is precocious puberty more likely

A

females (90% of cases)

115
Q

what is idiopathic cpp (central precocious puberty) and what do you have to rule out

A

early onset of puberty where the cause is not readily identifiable or is unknown

rule out brain tumour

116
Q

what is true precocious puberty, with what test is it diagnosed, and how is it treated

A

“True precocious puberty” refers to the early onset of puberty caused by the premature activation of the hypothalamic-pituitary-gonadal axis, leading to the development of secondary sexual characteristics before the usual age range for puberty.

diagnosed by measuring levels of LH and FSH
treated with GnRH super antagonist

117
Q

what is Hypogonadotrophic hypogonadism

A

sexual infantilism related to to gonadotrophin
deficiency

118
Q

what is Hypergonadotrophic hypogonadism

A

This condition involves dysfunction in the gonads themselves, resulting in the failure of the gonads to produce adequate sex hormones. As a compensatory mechanism, the pituitary gland secretes higher-than-normal levels of LH and FSH.

119
Q

when should you investigate boys or girls for pubertal delay

A

Girls
* Lack of breast development by 13 yrs
* More than five years between breast development and menarche
* Lack of pubic hair by age 14 yrs
* Absent menarche by age 15-16 yrs

Boys
* Lack of testicular enlargement by age 14 yrs
* Lack of pubic hair by age 15 yrs
* More than 5 years to complete genital enlargement

120
Q

what lab tests would you run on someone with signs of delayed puberty?

A

Complete red blood count
U&E, renal, LFT (liver function tests), coeliac antibodies
LH, FSH
Testosterone/ Oestradiol
Thyroid function
Prolactin
DHEA-S, ACTH, Cortisol

121
Q

what are possible causes of pubertal delay

A

Chronic renal disease
Chronic lung disease
Anorexia nervosa
Bulimia
Extreme exercise
Psychosocial/ stress
Drugs
Sickle cell disease
Cushing’s
Hypothyroidism
poorly controlled T1D

122
Q

what is the difference between primary secondary and tertiary hypogonadism?

A

Primary Hypogonadism: Dysfunction at the gonadal level leading to reduced production of sex hormones directly from the gonadal tissue itself.

Secondary Hypogonadism: Dysfunction at the pituitary gland or hypothalamus level, resulting in reduced stimulation of the gonads by pituitary hormones (LH and FSH).

Tertiary Hypogonadism: Dysfunction at the hypothalamus level, impacting the release of Gonadotropin-Releasing Hormone (GnRH), which normally stimulates the pituitary gland to release LH and FSH.

123
Q

what is Klinefelter’s syndrome and what type of hypogonadism is it

A

primary hypogonadism
it is a genetic disorder of trisomy in the sex chromosomes (2x, 1y)
patients with Klinefelter’s have azoospermia (no sperm in their ejaculate)

124
Q

what is Turner’s syndrome, what kind of hypogonadism is it, and how does it present

A

hypergonadotrophic hypogonadism
genetic condition where ther is only 1 sex chromosome (1x), so the patient has 45 instead of 46 chromosomes in total

(chromosome number: 45,X0)

Presentation
Renal malformations – horseshoe kidney (fusion of the kidney)
Short stature
Cardiovascular malformations – aortic arch, spontaneous rupture

125
Q

where are the osmoreceptors located and how are those areas related to vasopressin

A

osmoreceptors are primarily located in the hypothalamus, specifically in a region called the supraoptic nuclei and the paraventricular nuclei of the hypothalamus.

the supraoptic and paraventricular nucleus in the hypothalamus synthesise ADH and oxytocin

126
Q

what controls ADH release

A

osmoreceptors in hypothalamus for day-to-day regulation
baroreceptors in brainstem and aortic arch for emergency

127
Q

how much of the human body is fluid

A

60%

128
Q

make a tree diagram of all of the water compartments and what proportion they are of the total body water of a 70kg human

A

42L in total
Intracellular fluid
2/3 total body water (28L)

Extracellular fluid
1/3 total body water (14L)

Extracellular divides into
Intravascular fluid and interstitial fluid

Intravascular fluid
1/4 ECF (3.5L)
Interstitial fluid
3/4 ECF (10.5L)

129
Q

write out which ions are most prevalent in intra and extracellular fluid compartments and explain how the charge balance is kept equal.

A

1) extracellular
cations: Na+ , Ca2+
anions: Cl-, HCO3-

2) intracellular
cations: K+ , Mg+2
anions: PO4-3, proteins

the intra and extracellular compartments are kept at a neutral charge by balancing out the cations and anions

130
Q

where does ADH bind and how does it complete its function?

A

V2 receptor on principal cells of collecting duct –> increases H2O permeability by adding aquaporins

131
Q

what is osmolality

A

Concentration per kilo
different to osmolaRity because plasma volume also made up by lipids and proteins —> ads to the weight

132
Q

how do you calculate plasma osmolalilty at bedside and what is the normal osmolality

A

2xNa + Glucose + urea
K+ is excluded because because of incomplete dissociation of NaCl

Normal osmolality: 282-295 mOsmol/kg

133
Q

Calculate the osmolality of the patient with the blood results below and say wether they are normal, hyponatremic or hypernatremic

Na+ = 125 mmol/L
Glucose = 4.5 mmol/L
Urea = 6 mmol/L

A

2xNa + Glucose + urea

Total = 260.5

Hyponatremic

134
Q

What are AVP deficiency and resistance symptoms and how do you diagnose it

A

polyuria - you can’t mobilise aquaporins so the water can’t be reabsorbed
polydipsia - too much drinking water
no glycosuria

Diagnosis
measure urine volume >3L per day
check renal fuction and serum calcium
inappropriately dilute urine <200 mmol/L
serum osmolarity > 300polyuria - you can’t mobilise aquaporins so the water can’t be reabsorbed
polydipsia - too much drinking water
no glycosuria

Diagnosis
measure urine volume >3L per day
check renal fuction and serum calcium
inappropriately dilute urine <200 mOsmol/kg
serum osmolarity > 300 mOsmol/kg (hypernatremia)

135
Q

what are the causes of cranial diabetes insipidus

A

think making too little ADH
idiopathic, hpothalamic/posterior pit tumorus, trauma, infections(TB, meningitis), aneurysm next to pituitary , sickle cell, genetic, autoimmune

136
Q

what are causes of nephrogenic diabetes insipidus

A

think being resistant to ADH
genetic, diabetes mellitus, drugs, chronic renal impairment, post-obstructive nephropathy, metabolic hypercalcaemia and hypokalemia

diabetes mellitus cuz of high blood sugar > damage to cap and nephr

for hypercalcaemia and hypokalemia mechanism is not well known - just memorize

remember that K decreases urinary Ca excretion –> increases body Ca levels

137
Q

what is the water deprivation test and what are the the expcted results for AVP resistance vs AVP deficiency

A

it is a test where the patient is deprived from water and the plasma and urine concentrations are measured to observe the actions of AVP

in AVP resistance because the body doesn’t respond to ADH you won’t have water being taken form urine to blood so you end up with high plasma concentration and low urine concentration cuz too much water excreted

in AVP deficiency you just don’t produce enough ADH so it will decrease plasma concentration and increase urine concentration, but much slower and will not reach the normal levels anyways.

138
Q

what is an alternative soution to water deprivation tests

A

hypertonic saline infusion and measurement of AVP

139
Q

how do you treat cranial diabetes insipidus

A

desmopressin

140
Q

how do you manage nephrogenic diabetes insipidus

A

try and avoid precipitating drugs
desmopressin

141
Q

what is the most common cause of hyponatremia and what serum sodium concentration defines SEVERE hyponatremia

A

excess diuretic use
serum sodium < 125 mmol/L

142
Q

what is the value for normal serum sodium

A

135-144 mmol

142
Q

symptoms of hyponatremia

A

headache
irritability
nausea/vomiting
mental slowing
unstable balance
confusion/delirium
disorientation
coma
convulsions
respiratory arrest

143
Q

how does the brain structure change in response to hyponatremia or hypernatremia

A

the brain changes size
hyponatremia —> shrinks
hypernatremia —> inflates

144
Q

what tests do you run when you suspect hyponatremia in a patient

A

Plasma osmolality
Urine osmolality
Plasma glucose
Urine sodium
Cortisol —> ?
Thyroid function tests —> ?
Assesment of other causes like chest imaging

why do you need urine sodium AND urine osmolality

145
Q

what is syndrome of antidiuresis (SIAD) and how does it present

A

too much AVP being secreted
low plasma Na
high urine concentration
water retention - ECF volume increase
increase GFR but with less Na reabsorption cuz volume is high
urine Na > 30 mmol/L

146
Q

what are causes of SIAD

A

Cancers
Small cell lung carcinoma most common —> tumours can be ADH secreting

Central nervous system problems
head injury
brain tumour
Meningitis and encephalitis

Resp causes
Pneumonia
Tuberculosis
Severe Asthma
Pneumothorax
Emphysema

Drugs
opioids
Chlorpropamide
Carbamazepine
Vincristine

147
Q

Treatment of SIAD

A

fluid restriction to less than 1L/24h
is Na <115mmol/L fit hypertonic saline

Demeclocycline – inhibits action of vasopressin on kidney

Vasopressin receptor antagonists (vaptans) – V2 blocker

Tolvaptan – used for treatment of hyponatraemia secondary to SIADH as promotes water excretion with no loss of electrolytes

148
Q

what is osmotic demyelination syndrome?

A

massive demyelination of descending axons and pons and of brain due to severe hyponatremia
This condition often arises due to rapid shifts in serum osmolarity

149
Q

what are risk factors for osmotic demyelination syndrome

A

hyponatremia
hypokalemia
chronic excess alcohol
malnutrition
advanced liver disease

150
Q

does diabetes insipidus present with glycosuria
explain

A

no because this form of diabetes isn’t due to too much glucose circulating in blood but due to ADH deficiency/resistance so you pee too much but you won t have too much glucose in urine

youhave normal blood glucose levels

151
Q

what is goitre and what generally causes it

A

palpable and visible thyroid enlargement

commonly sporadic and autoimmune

152
Q

what is hyperthyroidism and what are the possible mechanism for hyperthroidism

A

excess of thyroid hormones in blood

3 mechanisms:
a. overproduction thyroid hormone

b. leakage of preformed hormone from thyroid

c. ingestion of excess thyroid hormone

153
Q

what is the most common cause of hyperthyroidism

A

Grave’s disease

154
Q

what in the biggest risk factor to developing thyroid autoimmunity

A

being female

155
Q

what is grave’s disease

A

Body produces antibodies which mimic the shape of TSH molecules - TRAb

They stimulate the TSH receptors. Thus, the body thinks that it has to produce more thyroid hormone but the stimulus is not actually TSH.

156
Q

what is multi-nodular goitre

A

thyroid forms nodules which work independently from the thyroid feedback system –> end up with more thyroid hormone than you would need

157
Q

what is exophthalmos and what diseases is it associated with

A

bulging and swelling of eyeball
characterised by hypertrophy of eyeball tissue

associated with grave’s disease and some autoimmune hypothyroidism patients

158
Q

what is the general presentation of a patient with hyperthyroidism

A

irritable
anxious
sweating
heat intolerance
increased HR
low weight regardless of how much they eat
fatigue
diarrhoea
menstrual disturbance

159
Q

what is the most common cause of solitary toxic thyroid nodule

A

benign adenoma

160
Q

what are the different presentations of goitre

A

diffuse, multi nodular, solitary nodule

161
Q

what is the mechanism of action of autoimmune hypothyroidism

A

body forms antibodies against thyroglobulin and thyroid peroxidase

162
Q

what is Hashimoto’s thyroiditis and what is the main pathological mechanism

A

cytotoxic T cells recognise and attach thyroid cells

163
Q

what are the mechanisms of secondary damage in Hashimoto’s

A

body forms antibodies against Thyroglobulin and thyroid peroxidase (TPO)

Uncommonly antibodies against the TSH-receptor may block the effects of TSH

164
Q

how can grave’s disease be a cause of hyperthyroidism

A

the TSH receptor antibodies stimulate the the thyroid to produce more thyroid hormone

165
Q

what are environmental risk factors for developing thyroid autoimmunity

A

stress, high iodine intake and smoking, radioactive exposure

166
Q

what is an example of an autoimmune disease which is associated with thyroid autoimmunity

A

type 1 diabetes mellitus

167
Q

how can grave’s cause foetal hyperthyroidism

A

the TSH-R (receptor) antibodies can cross the placenta and cause excessive thyroid hormone production in the foetus

168
Q

what are the most common causes of hyperthyroidism

A

grave’s disease
toxic multi nodular goitre
toxic adenoma (solitary nodule)
pituitary adenoma
neonatal hyperthyroidism
hereditary
iodine induced hyperthyroidism

169
Q

what are the clinical signs of grave’s disease

A

diffuse goitre
exophthalmos
pretibial myxoedema
acropachy

170
Q

what is the clinical sign of thyroid adenoma

A

solitary nodule

171
Q

what investigations would you do in a patient who presents with goitre

A

thyroid function tests –> t4, t3 and TSH
measuring thyroid antibodies for TPO, thyroglobulin and TSH-R antibody
Thyroid ultrasound
Radioactive iodine isotope uptake scan

172
Q

what patterns do you expect to see in t4, t3 and TSH amounts in primary hyperthyroidism vs secondary hyperthyroidism

A

primary hyperthyroidism: increased t4 and t3 but decreased TSH

in secondary hyperthyroidism you expect increased t4 and t3 and TSH

173
Q

what are possible treatments of hyperthyroidism

A
  • antithyroid drugs –> CARBIMAZOLE
  • radio-iodine
  • surgery –> partial or total thyroidectomy
174
Q

what is the 1st line of treatment for hyperthyroidism

what is the drug’s mechanism of action

what is the class of the drug

A

carbimazole - decreases synthesis of new thyroid hormone and suppresses immune system

class: thionamides

175
Q

what is a word for normal thyroid state

A

euthyroidism

176
Q

what are the 2 possible regimens of thionamide administration

A

there are 2 options:
1) they are administered over 12-18 months and they are slowly reduced more and more as thyroid function improves to avoid hypothyroidism –> TITRATION REGIMEN

2) they are administered in a high dose to stop thyroid hormone production completely and synthetic T4 is administered to maintain normal thyroid levels –> BLOCK AND REPLACE regimen

177
Q

what is a severe side effect of carbimazole

A

AGRANULOCYTOSIS –> loss of white blood cell granulocytes (ex.: neutrophils)

178
Q

explain what is the radio iodine therapy and what are possible complications and contraindications

A

Radioactive iodine taken up and local irradiation and tissue damage causes return to normal function

Could potentially lead to hypothyroidism

Contraindicated in pregnancy and breast feeding

179
Q

describe primary, secondary and tertiary hypothyroidism

A

primary –> absence or dysfunction of thyroid gland
secondary –> due to problem with pituitary
tertiary –> due to problem with hypothalamus

180
Q

what are causes of hypothyroidism

A

Hashimoto’s thyroiditis
131I therapy
Thyroidectomy
Postpartum thyroiditis
Thyroid hormone resistance
Pituitary disease
Hypothalamic disease
drug

181
Q

what are possible drug causes of hypothyroidism

A

Carbimazole
Lithium
Amiodarone - Can cause HYPERthyroidism due to high iodine and HYPOthyroidism as it inhibits the conversion of T4 to T3
Interferon

182
Q

what are the clinical features of hypothyroidism

A

tired
weight gain
Cold intolerance
Constipation
Menstrual disturbance
Muscle cramps
decreased cognition
Dry, rough skin
Periorbital oedema
Delayed muscle reflexes
Oedema

183
Q

what levels of TSH, t3 and t4 would you expect to see in primary and secondary hypothyroidism

A

primary –> increased TSH and decreased T4 and T3

secondary –> TSH, t3 and t4 very low

184
Q

how do you treat hypothyroidism

A

synthetic l-thyroxine (T4)

185
Q

what is the usual starting dose for thyroid hormone replacement therapy and how is it adjusted over time

A

100 micrograms

it is titrated over time based on thyroid function test results

check levels 6-8 weeks after dose adjustment

186
Q

what are possible causes of neonatal hypothyroidism

A
  • Thyroid agenesis > thyroid doesn’t form at all
  • Thyroid ectopia > thyroid forms in a werid place in the body
  • Thyroid dyshormonogenesis > genetic defects which affect the synthesis of thyroid hormones
  • Resistance to thyroid hormone
  • Isolated TSH deficiency
187
Q

what are the 3 main problems a pituitary adenoma could cause

A

1) mass effects
- visual disturbances
- headaches
- cranial nerve palsy and temporal lobe epilepsy
- CSF rhinorrhoea
2) increase hormone levels
3) decrease hormone levels

188
Q

what is the surgical procedure for pituitary tumours?

A

trans-sphenoidal surgery

189
Q

how are non-functioning pituitary tumours different to functioning pituitary tumours?

A

no hormone secretion

190
Q

how do you test the pituitary function?

A

measure GH, LH/FSH, ACTH, TSH and ADH

191
Q

what is acromegaly

A

Acromegaly = excessive production of growth hormone occurring in adults after fusion of the epiphyseal plates

192
Q

what is gigantism

A

Gigantism = excessive production of growth hormone occurring in children before fusion of the epiphyses of long bones

193
Q

what are the presenting clinical features of acromegaly

A

acral enlargement
arthralgias–> joint stiffness
maxillofacial changes
excessive sweating
headache
hypogonadal symptoms

194
Q

what are the options for treatment in acromegaly

A

transsphenoidal pituitary surgery
radiotherapy
medical therapy with:
1) somatostatin analogues (IM octreotide/lanreotide)
2)Dopamine agonists (oral bromocriptine/cabergoline),
3) GH anatagonists (pegvisomant)

195
Q

what are some complications of transsphenoidal pituitary surgery

A

Hypopituitarism
Death
Diabetes insipidus
infection
nasal septum perforation

196
Q

what causes prolactinoma

A

lactotroph cell tumour of pituitary

197
Q

what are the effects of too much prolactin

A

menstrual irregularity/amenorrhoea
infertility
galactorrhoea
low libido
low testosterone in men

198
Q

causes of hyperprolactinaemia

A
  • prolactin secreting pituitary adenoma (prolactinoma)
  • Other tumours may also cause high prolactin by inhibiting dopamine and so reducing its inhibitory effects on prolactin
  • primary hyperthyroidism (high TSH stimulates prolactin)
  • Drugs such as oestrogens, metoclopramide can also cause it
199
Q

how do you treat prolactinomas

A

NEVER surgery
you only use medications

  • dopamine agonists (cabergoline and bromocriptine)
200
Q

explain how acromegaly could lead to diabetes via insulin resistance

A

acromegaly is caused by too high levels of GH which promotes increased blood glucose levels. insulin isn’t capable to manage these constant high glucose levels and in the end the pancreas cells are affected –> insulin resistance

201
Q

what characterises Cushing’s syndrome and what are possible causes

A

glucocorticoid excess

caused by pituitary or adrenal lesions

202
Q

what are signs of cushing’s

A

red purple striae
proximal myopathy
fractures
Hyperandrogenism, Hirsutism, Acne

203
Q

conn’s syndrome vs congenital adrenal hyperplasia

A

Conn’s syndrome refers ONLY to PRIMARY Aldosterone producing adenoma

is a genetic disorder that affects the adrenal glands’ ability to produce cortisol and aldosterone, two vital hormones involved in regulating various body functions.

CAH is caused by a deficiency of enzymes necessary for the production of cortisol in the adrenal glands. This deficiency leads to a buildup of certain hormones that are precursors to cortisol, causing an overstimulation of the adrenal glands. As a result, the adrenal glands grow larger (hyperplasia) in an attempt to produce more cortisol, hence the term “adrenal hyperplasia.”

204
Q

what is PPGL

A

Pheochromocytoma and Paraganglioma

it is rare tumour that can be inside or outside of adrenal glands and it is catecholamine secreting (adrenaline and noradrenaline)

204
Q

what are the 3 main clinical features of someone with type 1 diabetes

A

weight loss
moderate to high urinary ketones
many severe symptoms in a short time span

204
Q

what are the signs of diabetic ketoacidosis

A

hyperventilation (Kussmaul breathing)
dehydration (average fluid loss 5-6 litres)
hypotension
Tachycardia
coma

204
Q

what are the clinical features of diabetic ketoacidosis

A

polyuria and polydipsia
nausea and vomiting
weight loss
weakness
abdominal pain (confused with surgical abdomen)
Drowsiness / confusion

205
Q

what is MODY diabetes

A

Maturity-onset diabetes of the young
it is the most common type of monogenic diabetes –> SINGLE GENE defect altering beta cell function

it is like type 1 but at a more mature age than normal type 1

206
Q

MODY vs type 1 diabetes

A

Type 1
autoimmune condition
body’s immune system mistakenly attacks and destroys the insulin-producing cells (beta cells) in the pancreas –> complete lack of insulin production.

MODY (Maturity-Onset Diabetes of the Young):
It’s a rare genetic form of diabetes caused by mutations in specific genes that affect insulin production or function in the pancreas.

207
Q

what is Permanent Neonatal Diabetes

A

mutations prevent closure of kir 6.2 channel and therefore beta cells are unable to secrete insulin

208
Q

What endocrine diseases can lead to development of diabetes

A

acromegaly, cushing’s, pheochromocytoma

209
Q

how do you manage diabetic ketoacidosis

A

rehydration (3L first 3 hrs)

insulin (inhibits lipolysis, ketogenesis, acidosis, reduces hepatic glucose production, increase tissue glucose uptake)

replacement of electrolytes (K+)

210
Q

what are the complications of DKA

A

cerebral oedema (deterioration in consciousness level)
children more at risk

adult respiratory distress syndrome

thromboembolism – venous and arterial

aspiration pneumonia (in drowsy/comatose patients)

death

diabetic ketoacidosis

211
Q

do patients with type 1 diabetes have any C-peptide after a couple of years? why?

A

no because type 1 is due to complete wipeout of beta cells (autoimmune) –> you will have no more c-peptide

212
Q

what problems do too many fatty acids cause in the blood in diabetes

A

impair glucose uptake
provide energy for gluconeogenesis in liver –> more hyperglycaemia
form ketone bodies –> metabolic acidosis

213
Q

why is it important to monitor potassium levels in DKA patients

A

because the role of insulin is not only to move glucose into cells but also potassium –> patients with DK will also present with hyperkalemia and if you start treating them too aggressively with insulin then all K+ will go into cells and you will have hypokalemia –> serious arrhythmias and neurological problems

you might have to provide IV potassium to maintain normal blood potassium levels

214
Q

how do you treat DKA

A

Give fluids for REHYDRATION
Insulin
Replace electrolytes (like K+)

215
Q

what are possible DKA complications?

A

1) respiratory distress
2) cerebral oedema
3) thromboembolism (blood becomes more prone to clotting because of changes in viscosity, increased platelet activity and inflammation)
4) aspiration pneumonia (breathing vomit when consciousness is lost and getting an infection)
5) death

216
Q

at what blood glucose level do patients start showing behavioural and neural changes

A

less than 2.8 mmol/L

217
Q

what are the symptoms of hyperglycaemia?

A

shaking
tachycardia
sweating
dizziness
anxious
impaired vision

not polyuria or polydypsia because the question refers to short term

218
Q

what is the physiological response to hypoglycaemia?

A

release of glucagon, adrenaline
inhibition of insulin secretion

219
Q

what are closed-loop systems

A

machines which automate insulin delivery; they constantly monitor glucose levels and aim to function like a healthy pancreas; they provide more precise insulin dosing according to changing glucose levels

220
Q

what are the 2 tests for neuro-muscular irritability in hypocalcemia?

A

Chvostek’s sign
Trousseau’s sign

221
Q

what type of antibody is TRAb and what is it

A

IgG
produced in Grave’s
Thyroid Receptor Ab

222
Q

How is Metformin excreted?

A

Metformin is cleared by active tubular secretion and is excreted unchanged in the urine.

223
Q

What precautions do you need to take if a patient on metformin is undergoing a radiological investigation with iv contrast?

A

There is a risk of lactic acidosis in patients given iv contrast who are on Metformin, which has a mortality of 30-50%. If a patient taking Metformin requires a radiological investigation with intravenous contrast the serum creatinine must be measured within the preceding month. If the creatinine is normal and a low volume of contrast (up to 100ml) is to be administered no special precaution is required. If more than 100mls of contrast is used iv or is given intra
arterially then the metformin should be withheld for 48 hours prior to the contrast. If the serum creatinine is raised and contrast is deemed necessary then the metformin should be withheld for 48 hours prior to and post-contrast and the serum creatinine should be measured prior to restarting the metformin.

224
Q

what is a serious side effect of amiodarone

A

amiodarone-induced thyrotoxicosis which leads to the destruction of the thyroid

225
Q

what is a SERIOUS side effect of carbimazole and how does it present

A

agranulocytosis –> SORE THROAT

226
Q

can you give carbimazole to pregnant women? if yes say why and if no offer the alternative

A

NOOOOOO –> it is highly teratogenic
alternative: propylthiouracil

227
Q

what is the block and replace strategy for treating hyperthyroidism and why is it done

A

Block-replace → management strategy to block thyroid hormone production and replace thyroid hormones with thyroid replacement therapy: give carbimazole + levothyroxine simultaneously (less risk of iatrogenic hypothyroidism).

228
Q

what is a MASSIVE complication of hyperthyroidism. describe it, what could cause it and treatment

A

Thyroid storm –> Very high T4 levels
Hyperpyrexia
Tachycardia
Extreme restlessness
Even delirium, coma and death

Usually precipitated by
Infection
Stress
Surgery
Radioactive iodine therapy

Treatment
Large doses of Carbimazole
Propranolol - beta blocker to prevent arrhythmias
Potassium iodide – to acutely block release of thyroid hormone from gland
Hydrocortisone – to inhibit peripheral conversion of T4 to T3

229
Q
A

phase 2 medicine (15 decks)

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