Brainscape's Knowledge GenomeTM

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


See full index

Phase 2a - Jemima > ENDOCRINOLOGY > Flashcards

ENDOCRINOLOGY Flashcards

1
Q

what are the major endocrine constituents

A

pituitary gland, thyroid gland, parathyroid gland, adrenal glands, pancreas, ovaries and testes

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

what are the features of water soluble hormones

A

they are unbound, and bind to cell surface receptors. They have a short half life and clearance is fast.

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

what are examples of water soluble hormones

A

peptides
monoamines - adrenaline/noradrenaline

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

what are the features of fat soluble hormones

A

they are protein bound, and diffuse into the cell. they have a long half-life and clearance of them is slow

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

what are examples of fat soluble hormones

A

Thyroid hormones
steroids

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

can peptide hormones be stored

A

yes they can be stored in vesicles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what are the steps of peptide production from synthesis to secretion

A

synthesis - preprohormone into prohormone
packaging - prohormone to hormone
storage - hormone
secretion - hormone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

are thyroid hormones water soluble

A

no they are not water soluble - 99% are protein bound

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what are the features of vitamin D

A

it is fat soluble, it enters the cell directly to the nucleus to stimulate mRNA production. It is transported round the body by vitamin D binding protein

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

what are some cholesterol derivative hormones

A
  1. vitamin K
  2. Adrenocorticoids
  3. Sex hormones
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what are features of adrenocortical and gonadal steroids

A

95% of them are protein bound and after entering the cell they pass into the nucleus to induce a response, binding to cytoplasmic receptors

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

what are the actions of steroid hormones

A
  1. steroid hormones diffuse through the plasma membrane and binds to receptors
  2. receptor - hormone complex enters the nucleus
  3. receptor - hormone complexes bind to the GRE
  4. binding initiates transcription of the gene to mRNA
  5. mRNA then becomes protien syntheis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

how does the body control hormone secretion

A
  • basal secretion; continuously or pulsatile
  • Negative feedback; i.e dopamine inhibits prolactin
  • releasing factors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

how does the body control hormone secretion

A
  • basal secretion; continuously or pulsatile
  • Negative feedback; i.e dopamine inhibits prolactin
  • releasing factors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

how does the body control hormone action

A
  1. hormone metabolism - increased metabolism to reduce function
  2. hormone receptor induction - induction of LH receptors by FSH in follicle
  3. hormone receptor down regulation - hormone secreted in large quantities cause down regulation of its target receptors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what is synergism

A

it is the combined effects of two hormones amplified

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

what is an example of hormone synergism in the body

A

glucagon with adrenaline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what is antagonism

A

one hormone opposes another hormone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what is an example of hormone antagonism

A

glucagon antagonises insulin

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

what can cause pituitary dysfunction

A
  1. tumour mass effects
  2. hormone excess
  3. hormone deficiency
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what is the hypothalamus - pituitary - thyroid axis

A

hypothalamus - TRH - anterior pituitary - TSH - thyroid gland - thyroid hormones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what is thyroid hormone function

A
  1. accelerates food metabolism
  2. increases protein synthesis
  3. enhances fat metabolism
  4. brain development during foetal life and postnatal development
  5. growth rate accelerated
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what steroid hormones does the adrenal cortex produce

A
  1. Mineralocorticoids - aldosterone
  2. Glucocorticoids - cortisol androgens
  3. Androgens - androstenedione and DHEA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what hormones do the adrenal medulla produce

A

produces adrenaline and noradrenaline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what is satiety

A

the feeling of fullness - disappearance of appetite after a meal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what are the different BMI groupings

A

<18.5 - underweight
18.5-24.5 - normal
25.0-29.9 - overweight
30.0-39.9 - obese
> 40 - morbidly obese

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

what are risks of obesity

A
  1. type 2 diabetes
  2. hypertension
  3. coronary artery disease
  4. stroke
  5. osteoarthritis
  6. obstructive sleep apnoea
  7. carcinoma: breast, endometrium, prostate, colon
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what are the reasons we eat

A
  • internal physiological drive to eat
  • feeling that prompts thought of food and motivates food consumption
  • external physiological drive to eat
  • sometimes even the absence of hunger
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what region of the brain which has a central role in appetite regulation

A

the hypothalamus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what nutrients have a quick short effect on satiety

A

highly refined sugar

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

what nutrients give a prolonged satiety

A

high protein foods

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

what nutrients can stimulate and entice people to eat more

A

high fat

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

what is peptide YY

A

it is a protein structurally similar to NPY binding to its receptors. and reduces appetite

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

what areas of the body produces peptide YY

A

it is secreted by neuroendocrine cells in the ileum, pancreas and colon in response to food

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

what is the function of peptide YY

A

it inhibits gastric motility and reduces appetite

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

what is the function of cholecystokinin

A

it delays gastric emptying, causes gall bladder contraction and insulin release
via the vagus nerve it induces satiety

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

where are CCK receptors found

A

in the pyloric sphincter

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

what stimulates appetite

A

olfactory, gustatory, cognitive and visual stimuli increase appetite

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

what hormone increases hunger

A

ghrelin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

what factors increase satiety to stop feeding

A

stretch receptors in the stomach
release of CCK, GLP, insulin and PYY

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

what are the anterior pituitary hormones

A

FSH and LH
ACTH
GH
TSH
Prolactin

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

what can pituitary tumours cause

A
  1. can press on local structures such as the optic chiasm producing bitemporal hemianopia
  2. Hyopituitism
  3. Hyperpituitism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

what does the posterior pituitary release

A

oxytocin
vasopressin

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

what are the functions of cortisol

A

increases protein and carbohydrate breakdown
it upregulates alpha receptors on arterioles and therefore increases blood pressure.
it suppresses the immune response
it increases osteoclast activity and therefore its osteoporotic
it increases insulin resistance

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

what is the definition of diabetes type 1

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
46
Q

what are risk factors for type 1 diabetes

A

HLA DR3-DQ2 or HLA DR4-DQ8
northern european
autoimmune diseases - 90%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

what is the pathophysiology of type 1 diabetes

A

autoantibodies attack beta cells in the islets of langerhans which causes an insulin deficiency and hyperglycaemia.
this causes continuous breakdown of glycogen from the liver due to gluconeogenesis and produces glycosuria

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

what are the signs and symptoms of diabetes type 1

A

Classic triad; polydipsia, polyuria, weight loss (BMI <25)
usually a short history of severe symptoms
may present with ketosis

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

how do you diagnose type 1 diabetes

A

In symptomatic patients you need to have a random plasma glucose of over 11mmol/L or a fasting blood glucose of over 7 mmol/L
In asymptomatic patients they must show raised glucose on 2 separate occasions

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

what is the treatment for type 1 diabetes

A
  1. insulin
  2. short - acting insulins and insulin analogues (4-6 hours)
  3. longer (basal) acting insulin (12-24 hours)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

what is the definition of type 2 diabetes

A

it is non insulin dependent
patients gradually become insulin resistant/pancreatic beta cells fail to secrete enough insulin or both. it progresses from an impaired glucose tolerance to diabetes.

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

what are the causes of type 2 diabetes

A

Non modifiable - Older age, ethnicity, family history male
Modifiable - obesity, sedentary lifestyle, high carbohydrate diet, hypertension

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

what are risk factors for type 2 diabetes

A

lifestyle factors: obesity, lack of exercise, calorie and alcohol excess
higher prevalence in asian men
above the age of 40 - later onset
hypertension

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

what are signs and symptoms of type 2 diabetes

A
  1. polydipsia
  2. polyuria
  3. glycosuria
  4. central obesity
  5. slower onset
  6. blurred vision
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

how does someone get diagnosed with type 2 diabetes

A
  • fasting plasma glucose: more than 7mmol/L
  • random plasma glucose: more an 11 mmol/L
  • HbA1c more than 48 mmol/L - GOLD STANDARD
  • if someone has no symptoms - GTT 75g glucose, fasting over 7 or 2hr value over 11mmol/l which is repeated on 2 occasions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

what is first line lifestyle changes for type 2 diabetes

A
  1. dietary advice; high in complex carbs and low in fat
  2. smoking cessation
  3. decrease in alcohol intake
  4. encourage exercise
  5. regular blood glucose and HbA1c monitoring
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

what is second line management for type 2 diabetes

A

Medications
1. metformin: increases insulin sensitivity - first choice for overweight patients
2. If HbA1c remains high then dual therapy with metformin:
- DPP4 inhibitor
- Sulphonylurea - increases insulin secretion
- Pioglitiazone
3. if still high then you have triple therapy
4. then insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

what is diabetic ketoacidosis

A

when complete lack of insulin results in high ketone production
- medical emergency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

what sort of release does insulin have

A

a biphasic release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

what receptors does glucose bind to in the pancreas

A

binds to the GLUT2 receptors (B cells) stimulating insulin release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

what happens when insulin binds to peripheral insulin receptors

A
  1. it activates intracellular tyrosine kinases and its cascade
  2. it results in increased GLUT4 channel expression on the cell surface membrane
  3. it increases peripheral uptake
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

what is given in response to unresponsive hypoglycemic patients

A

IM glucagon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

what does oxytocin do

A

causes milk ejection and labour induction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

what does vasopressin do

A

increases blood pressure
- vasoconstriction
- APO II expression in CD
- increased aldosterone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

what are complications of diabetic ketoacidosis

A
  1. coma
  2. cerebral oedema
  3. thromboembolism
  4. aspiration pneumonia
  5. death
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

how do you manage diabetic ketoacidosis

A

ABC
- replace fluid loss with 0.9% saline IV
- IV insulin + glucose to prevent hypoglycaemia
- Restore electrolytes such as K+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

what does post prandial mean

A

means after eating

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

how do beta and alpha cells act on each other

A

the beta cells keep the alpha cells in a state of tonic inhibition when there is high glucose. this is opposed with reduced glucose levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

simply how does glucose act on beta cells in the pancreas

A

glucose binds to GLUT2 receptors on beta cells. Through intracellular signaling it causes ADP transformation into ATP. This induces closure of potassium channels causing depolarisation of the membrane. This causes calcium channels to open and calcium moves into the cell, causing insulin secretory granules to be released from the cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

how does insulin act on peripheral receptors

A

insulin binds to its receptor and induces intracellular GLUT4 vesicles to be mobilised to the membrane, allowing glucose to bind and enter the cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

what does HbA1c show

A

it shows a trend over time - how much glucose is stuck in a red blood cell can tell you the two/three month blood sugar

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

what is the threshold of when glucose starts appearing in the urine

A

anything above 10-11mmol/L of glucose in the blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

which type of diabetes is ketoacidosis more common in

A

type 1 but you can get it late stage type 2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

what is a hyperosmolar hyperglycaemic state

A

it is common in type 2 diabetes. It is where the kidneys become dehydrated (even through you are drinking a lot). The kindeys eventually go into kidney failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

what is the pathogenesis of type 1 diabetes

A

there is absent insulin secretion, meaning you have no fat, muscle or hepatic insulin effect. Because of this you have impaired glucose clearance and muscle fat breakdown. You also have unrestrained glucose and ketone production. More glucose enters the blood with a lack of it being taken up by peripheral tissues and you end up with hyperglycaemia and raised ketones in the blood and urine. Will eventually become ketoacidotic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

what is the pathogenesis of type 2 diabetes

A

Repeated exposure to high levels of glucose leads to the repeated release of insulin which makes the cells in the body become resistant to the effects of insulin.
Over time, the pancreas (specifically the beta cells) becomes fatigued and damaged by producing so much insulin and they start to produce less.
A continued onslaught of glucose on the body in light of insulin resistance and pancreatic fatigue leads to chronic hyperglycaemia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

what is the action of sulphonylureas

A

they depolarise the calcium channel allowing calcium channels to open and increase insulin release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

what are side effects of sulphonylureas

A

they can cause hypoglycaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

how do thiazolidinediones work

A

they bind to the nuclear receptor PPARy and activates genes which a concerned with glucose uptake and utilisation, as well as lipid metabolism
- help improve insulin sensitivity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

what are side effects of thiazolidinediones

A

they can increase weight, increase the risk of heart failure and increase the risk of fractures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Where is GLP-1 secreted from

A

secreted from the L cells in the intestine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

What are the modes of action of GLP-1

A
  • stimulates insulin secretion
  • supresses glucagon secretion
  • slows gastric emptying
  • reduces food intake
  • increases beta cell mass and improves function
  • improves insulin sensitivity
  • enhances glucose disposal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

what actions do GLP-1 agonists have

A

they reduce food intake while stimulating insulin secretion, it can help reduce weight and CVD independent of lowering glucose levels
- incretin mimetic which inhibits glucagon secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

what is DPP - iv

A

it breaks down GLP-1 and stops its affects on the body
Also increases incretin levels which inhibits glucagon secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

what are examples of DPP - iv inhibitors

A

Vildagliptin and sitagliptin
- oral agents and have a modest glucose lowering effect. they have no effect on CVD or weight

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

what is the action of SGLT2 inhibitors

A

inhibit the glucose reuptake transporters in the nephron. this means that all glucose is urinated out which will then reduce blood glucose and reduce patient symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

what is the action of SGLT2 inhibitors

A

inhibit the glucose reuptake transporters in the nephron. this means that all glucose is urinated out which will then reduce blood glucose and reduce patient symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

what are examples of SGLT2 inhibitors

A

empagliflozin, canagliflozin and dapagliflozin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

what are side effects of SGLT2 inhibitors

A

genital thrush, UTIs and dehydration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

what are benefits of SGLT2 inhibitors

A

they significantly reduce heart failure, heart attacks and kidney disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

what are the two types of insulin given in diabetes

A

long and short acting
- basal insulin is long lasting
- bolus gives a spike which can be taken before dinner

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

what are some examples of basal insulin

A

NPH insulin, insulin glargine, insulin detemir, insulin degludec

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

what are some examples of prandial insulins

A

insulin lispro, insulin glulisine, EDTA/citrate human insulin and faster-acting insulin aspart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

how many people with type 2 diabetes will end up on insulin after 10 years

A

about 50%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

what are the classifications for hypoglycaemia

A

Level 1 - alert value, plasma glucose below 3.9mmol/L and no symptoms
Level 2 - serious biochemical, plasma glucose <3mmol/L

Non severe vs severe symptomatic:
Non severe: patient has symptoms but self treated and cognitive
Severe: patient has impaired cognitive function and required external help to recover

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

what are the side effects of hypoglycaemia

A

brain - cognitive dysfunction, backouts, seizures, comas
musculoskeletal - falls, accidents, fractures, dislocations
heart - myocardial ischemia, arrhythmias
circulation - inflammation, blood coagulation abnormal, haemodynamic changes, endothelial dysfunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

what are common hypoglycaemic symptoms

A
  1. autonomic: trembling, sweating, palpitations, anxiety, hunger
  2. Neuro: confusion, weakness, dizziness, drowsiness, vision and speech difficulty, difficulty concentrating
  3. non-specific: nausea and headache
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

what happens if you have repeated episodes of hypoglycaemia

A

youre awareness to the adrenaline response becomes progressively blunted. you can eventually loose the awareness. this can be combatted if you can avoid hypoglycaemia for as little as 4-6 weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

where is the glucose sensor in the brain

A

in the ventral medial hypothalamus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

what are causes of hypoglycaemia

A

long duration of having diabetes
increasing age
increased physical activity
sleeping
use of drugs - prescribed or alcohol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

What is MODY diabetes

A

maturity onset diabetes of youths
- rare T2DM presenting in young patients

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

what are some secondary causes of diabetes

A
  • acromegaly and cushings
  • haemochromotosis
  • thiazides/corticosteroids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

what is LADA diabetes

A

it is late onset of diabetes in adults
- the opposite of MODY; type 1 presentation in older patients

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

do you have a ‘pre-diabetes’ stage in type 1 diabetes

A

NO - no lifestyle modification will affect this disease development

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

what are symptoms of T1DM diabetic ketoacidosis

A
  • kussmaul breathing - deep laboured breaths
  • pear drop breath - fruity breath smell
  • reduced tissue turgor, hypotension and tachycardia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

how do you diagnose diabetic ketoacidosis

A

ketones (blood) = >3mmol/L
Hyperglycaemic > 11.1mmol/L RPG
Acidosis (met) <7.3pH or <15mmol HCO3-

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

what is the treatment for diabetic ketoacidosis

A

ABCDE
- first line is ALWAYS fluid and then insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

what are symptoms of type 2 diabetes

A
  • obese
  • hypertensive
  • older patient
  • polydipsia
  • polyphagia - excessive hunger
  • polyuria
  • glycosuria
  • can get dark pigmented skin folds
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

what are the blood measurements for pre-diabetic diabetes

A

IGT = normal FPG >6mmol/L and 2hr OGTT between 7.8-11mmol/L
IFG = F.PG 6.1-6.9mmol/L and 2hr OGTT <7.8mmol/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

what are main macrovascular and microvascular complications in DM1 and 2

A

Macrovascular: Cardiovascular, ischemic stroke, peripheral arterial (PVD)
Microvascular: retinopathy, neuropathy (charat foot), nephropathy (nephrotic syndrome)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

what are non diabetic reasons for hypoglycaemia

A

Oral, Liver failure and addisons disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

what spinal levels does the thyroid sit at

A

C5-T1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

what connects the two lobes of the thymus

A

the Isthmus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

where does the anterior pituitary receive its blood supply from

A

receives its blood from the portal venous circulation from the hypothalamus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

describe the growth hormone/IGF-1 axis

A

The growth hormone/ IGF-I (insulin-like growth factor) axis begins at the hypothalamus which produces Growth Hormone Releasing Hormone (GHRH) or somatostatin (SMS), also known as growth hormone inhibiting hormone (GHIH). GHRH increases the amount of growth hormone produced by the pituitary, which then goes to the liver. GHIH decreases GH production from the pituitary so that less goes to the liver.
The liver produces IGF-I which reduces the production of GHRH.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

what is IGF-1

A

it is insulin like growth factor 1 and is produced by the liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

what stimulates growth hormone release from the pituitary

A

Growth hormone releasing hormone
- somatostatin inhibits

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

what stimulates LH and FSH release from the anterior pituitary

A

GnRH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

what stimulates ACTH release from the anterior pituitary

A

CRH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

What stimulates TSH release from the anterior pituitary

A

TRH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

What pituitary diseases can cause pituitary dysfunction

A
  • Benign pituitary adenoma
  • Craniopharyngioma
  • Trauma
  • Apoplexy/Sheehans - excessive blood loss
  • Sarcoid/TB
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

what are the three vital signs of presentation for diagnosing pituitary tumours

A
  1. Pressure on local structure (optic nerves) - bitemporal hemianopia
  2. Pressure on normal pituitary - hypopituitarism
  3. Functioning tumour: prolactinoma, Acromegaly, Cushings
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

how would someone present with a prolactinoma

A

galactorrhoea, amenorrhoea and infertility
loss of libido
visual field defects
low testosterone
erectile dysfunction
reduced facial hair

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

is a prolactinoma more common in men or women

A

more common in women

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

how do you treat a prolactinoma

A

treat with a dopamine agonist first

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

what is acromegaly

A

Acromegaly is a rare condition where the body produces too much growth hormone, causing body tissues and bones to grow more quickly. Over time, this leads to abnormally large hands and feet, and a wide range of other symptoms.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
127
Q

what are co-morbidities often related to acromegaly

A

hypertension and heart disease
cerebrovascular events and headache
arthritis
sleep apnoea
insulin - resistant diabetes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
128
Q

what are presenting clinical features of acromegaly

A
  • acral enlargement
  • arthralgias
  • amenorrhoea
  • bi-temporal hemianopia
  • maxillofacial changes
  • excessive sweating
  • headache
  • hypogonadal symptoms
  • can have visual field defects
  • lower pitch of voice
  • obstructive sleep apnoea
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q

what are the diagnosis steps for acromegaly

A
  • acromegaly is excluded if GH <0.4ng/ml and normal IGF-1
  • if either is abnormal then do 75gm glucose tolerance test
  • acromegaly excluded if IGF-1 normal and GTT <1ng/ml
    the gold standard of test is the oral glucose tolerance test - normally serum GH will decrease when given glucose but this wont happen in acromegaly
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
130
Q

what are treatment options for acromegaly

A
  1. pituitary surgery
  2. Medicine - dopamine agonists: cabergoline, somatostatin analogues: octreotide, GH receptor antagonists; Pegvisomant
  3. Radiotherapy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
131
Q

what is an example of a dopamine agonist used for acromegaly

A

cabergoline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
132
Q

what is the definition of a prolactinoma

A

lactotroph cell tumour of the pituitary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
133
Q

what are clinical features of a prolactinoma

A

local effects - headache, visual field defects, CSF leak
effect of prolactin - menstrual irregularity/amenorrhoea, infertility, galactorrhoea, low libido, low testosterone in men

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
134
Q

what is the management of a prolactinoma

A

medical rather than surgery, use dopamine agonists such as cabergoline.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
135
Q

what is a cardinal rhythm

A

physical, mental and behavioral changes that follow a daily cycle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
136
Q

what is adrenal insufficiency

A

a condition in which the adrenal glands do not produce adequate amounts of steroid hormone (mainly cortisol)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
137
Q

what are examples of primary, secondary and tertiary adrenal insufficiency

A

Primary - issue with gland itself - Addison’s disease
Secondary - Hypopituitarism
Tertiary - Suppression of HPA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
138
Q

how do you diagnose an adrenal insufficiency

A

Symptoms: fatigue, weight loss, poor recovery from illness, adrenal crisis, headache, vitiligo, hypoglycaemia
Past history: TB, post partum bleed, cancer
Family history: Autoimmunity, congenital disease
Gold standard is a Short synacthen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
139
Q

what is the treatment of adrenal insufficiency

A

steroids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
140
Q

what are the symptoms of an adrenal crisis

A
  • hypotension and cardiovascular collapse
  • fatigue
  • fever
  • hypoglycaemia
  • hyponatraemia and hyperkalaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
141
Q

whats somethings to think of when someone is presenting with adrenal insufficiency

A

recent steroid use

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
142
Q

what is the definition of hyperthyroidism

A

clinical effect of excess thyroid hormone.
primary - abnormal increased thyroid function
secondary - abnormal increased TSH production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
143
Q

what can cause hyperthyroidism

A

smoking
stress
HLA-DR3
other autoimmune conditions: T1DM, addisons and diabetes
Graves disease
Toxic multinodular goitre
iodine excess
De Quervains thyroiditis
Drug induced - iodine or amiodarone `

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
144
Q

what is the pathophysiology of hyperthyroidism

A

there is an increased T3 and T4 production, thus increasing the metabolic rate, cardiac output, bone resorption and activates the sympathetic nervous system
- feedback to pituitary and causes low TSH levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
145
Q

what are the different things that can cause hyperthyroidism

A

Graves disease - 65-75% of cases
autoimmune problems
toxic multinodular goitre
toxic adenoma
metastatic follicular thyroid cancer
iodine excess
secondary causes such as a TSH secreting pituitary tumour

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
146
Q

who is more likely to have hyperthyroidism

A

young women - 20-24yrs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
147
Q

what are the signs and symptoms of hyperthyroidism

A

everything goes fast
hot and sweaty
diarrhoea
hyperphagia
weight loss
palpitations
tremor
irritability
anxiety
oligomenorrhoea
goitre

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
148
Q

what investigations are done to diagnose hyperthyroidism

A
  • TFTs look at T3 and 4 and if it is increased, as well as if TSH is decreased (primary)
  • look for thyroid antibodies
  • Ultrasound and CT head
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
149
Q

what treatment is given for hyperthyroidism

A
  1. Drug management; beta blockers provide rapid symptom relief. 1st line carbimazole which blocks T4 synthesis, second like propylthiouracil which prevents T4 to T3 conversion
  2. radioiodine
  3. thyroidectomy (surgery)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
150
Q

what will TSH levels be like in secondary hyperthyroidism

A

they will be increased - problem with the pituitary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
151
Q

what hyperthyroid treatment shouldnt be given to pregnant women

A

carbimazole shouldnt be given

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
152
Q

what is the pathophysiology of graves disease

A

it is where IgG antibodies (anti-TSHR-Ab) bind to TSH receptors to increase T4/3 production
- also react with orbital autoantigens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
153
Q

what are symptoms other than hyperthyroidism which are associated with graves disease

A
  • Thyroid eye disease (25-50%); eyelid retraction, periorbital swelling and proptosis/exophthalmos
  • pretibial myxoedema (leg swelling and discolouration)
  • thyroid acropachy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
154
Q

what is the definition of hypothyroidism

A

is is the clinical effect of a lack of thyroid hormone
- primary is a abnormal reduction in thyroid function
- secondary is an abnormal reduction in TSH production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
155
Q

what is the epidemiology surrounding hypothyroidism

A
  • about 4/1000 per year and it is mostly in over 40s. it is also seen more commonly in women to men (6:1)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
156
Q

what are causes of hypothyroidism

A

Autoimmune causes - Hashimoto’s, primary atrophic hypothyroidism, De Quervans thyroiditis
Other primary causes - iodine deficiency drugs (antithyroid drugs, iodine, lithium), post thyroidectomy or radioiodine
secondary - hypopituitarism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
157
Q

what are signs and symptoms of hypothyroidism

A

everything goes slow
- fatigue
- weight gain
- loss of appetite
- cold
- lethargy
- constipation
- low mood and depression
- menorrhagia
- goitre

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
158
Q

what investigations are done to diagnose hypothyroidism

A

TFT - low T3 and T4 with an increased TSH
in secondary there will be a low TSH
also do blood test for autoantibodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
159
Q

what is the treatment for hypothyroidism

A

Levothyroxine - artificial T4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
160
Q

What is Cushing’s syndrome

A

long term exposure to excessive cortisol hormone which is released by the adrenals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
161
Q

what are causes of cushings syndrome

A

ACTH Dependent
- Cushings disease - ACTH secreting from pituitary adenoma
- Ectopic ACTH production from small cell lung cancer
ACTH Independent
- Iatrogenic - steroid use
- adrenal adenoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
162
Q

what are the signs and symptoms of cushings syndrome

A
  • moon face
  • central obesity
  • Buffalo hump
  • Acne
  • Hypertension
  • Striae - stretch marks
  • Hirsutism
  • weight gain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
163
Q

what investigations are done to determine if someone has Cushings syndrome

A
  1. random plasma cortisol (would be raised)
  2. Overnight dexamethasone suppression test - cortisol wont be suppressed in cushings
  3. Urinary free cortisol (24hr)
  4. Plasma ACTH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
164
Q

what are the treatment options for cushings syndrome

A

Dependent on the underlying cause
1. Latrogenic; stop medications if possible
2. Cushings disease - removal of the adenoma
3 Adrenal adenoma - adrenalectomy
4 Cortisol synthesis inhibition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
165
Q

what drugs are used to inhibit cortisol synthesis

A

metyrapone and ketoconazole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
166
Q

what are causes of acromegaly

A

pituitary tumour (adenoma) - most common 99%
secondary to a malignancy that secretes ectopic GH such as a lung cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
167
Q

what can be some complications of acromegaly

A

erectile dysfunction, diabetes mellitus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
168
Q

what is the pathophysiology of acromegaly

A

the overproduction of growth hormone acts directs on tissues such as the liver, muscle bone or fat and causes overgrowth of certain things like the hands and jaw, as well as causing other clinical features. GHRH is released from the hypothalamus and stimulates the release of GH from the anterior pituitary.
The excess growth hormone (GH) from the anterior pituitary results in excessive production of insulin like growth factor (IGF-1) which is responsible for inappropriate growth. This stimulates bone and soft tissue growth.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
169
Q

other than a prolactin producing tumour what are other reasons someone may develop hyperprolatinaemia

A
  • non functioning pituitary tumour compresses on the pituitary stalk and therefore there is no dopamine inhibition of prolactin release
  • antidopaminergic drugs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
170
Q

what are the two types of prolactinomas

A
  1. microtumours - less than 10mm in diameter (90%)
  2. macro - more than 10mm
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
171
Q

what investigations are done to diagnose a prolactinoma

A

blood test to see prolactin and a CT of the head

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
172
Q

what is Conn’s syndrome

A

it is primary hyperaldosteronism due to an aldosterone producing adenoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
173
Q

what is the pathophysiology of Conn’s syndrome

A

there is an excess production of aldosterone, independent of the RAA system
- there is high sodium and water retention
- there is increased potassium secretion
- there is low renin release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
174
Q

what are signs and symptoms of Conn’s syndrome

A

hypertension
hypokalaemia
nocturia
polyuria
mood disturbance
difficulty concentrating

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
175
Q

what investigations are done to diagnose conn’s syndrome

A
  • aldosterone-renin ratio blood test: increased
  • plasma potassium: reduced
  • U+E
  • Selective adrenal venous sampling (GOLD STANDARD)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
176
Q

what is the treatment for Conn’s syndrome

A

1st line: Spironolactone (pre-op controls BP and K+ levels)
Gold standard is laparoscopic adrenalectomy if its an adenoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
177
Q

what is the blood supply to the thyroid

A

the inferior and superior thyroid artery
- inferior from the thyrocervical trunk (subclavian)
- superior from the external carotid (ECA)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
178
Q

how is T3 and T4 made

A

iodine becomes trapped and diffuses into the colloid of the thyroid gland. This then binds to tyrosine residues on thyroglobulin using the TPO enzyme to form T1 or T2.
When TSH-R binding occurs it stimulates T1 or T2 release
- T1+T2=T3
- T2+T2=T4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
179
Q

what is the Graves triad

A
  • ophthalmopathy
  • dermopathy
  • acropachy - rash
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
180
Q

what are complications of hyperthyroidism

A

a thyroid storm - rapid deterioration of thyrotoxicosis and a mass increase in T4. causes systemic decompensation: AF, coma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
181
Q

what is treatment for a thyroid storm

A

propylthioruracil and KI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
182
Q

why do you need to be careful of when prescribing levothyroxine

A

not overprescribing, as the dose can often cause iatrogenic hyperthyroidism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
183
Q

what is a complication of hypothyroidism

A

myxedema coma - often infection precipitated. There is a rapid reduction in T4 which causes hypothermia, loss of consciousness and heart failure

184
Q

how do you treat a myxedema coma

A

levothyroxine, ABx and hydrocortisone (until adrenal insufficiency has been ruled out)

185
Q

what are the different types of thyroid carcinoma

A

papillary, follicular and anaplastic (worst prognosis), lymphoma and medullary cell

186
Q

what can a thyroid carcinoma mostly present as

A

they can present as thyroid nodules, and they may compress locally leading to a horse voice

187
Q

how would you diagnose a thyroid carcinoma

A

a fine needle aspiration biopsy - TFTs and ultrasound the thyroid

188
Q

what is the treatment for thyroid carcinoma

A

if its papillary and follicular = thyroidectomy, radioiodine
anaplastic = palliative mostly

189
Q

what is the difference between cushing disease and cushing syndrome

A

Cushing’s DISEASE = pituitary oedema secreting excess ACTH
Cushing’s SYNDROME = hypercortisolemia of any cause

190
Q

what blood tests are done when diagnosing Cushing’s

A

a random serum cortisol, if it is high then a second test is done measured at 12am. Cortisol is normally at its lowest here therefore if its high then its very abnormal

191
Q

what is the dexamethasone suppression test

A
  1. measure a patients cortisol and then give dexamethasone.
  2. measure cortisol levels 8hrs later
    - non-cushings = suppression of cortisol (>50nmol/L)
    - cushings - little to now suppression
192
Q

what is the dexamethasone suppression test looking at

A

dexamethasone is essentially cortisol, and therefore in a healthy patient there should be negative feedback when it is given, and reduce cortisol levels in the body

193
Q

what are complications of Cushing’s

A

osteoperosis
secondary diabetes mellitus
Hypertension
Cardiovascular disease

194
Q

what are the main causes of adrenal insufficiency

A

primary
developed world = autoantibody adrenal destruction (addison’s)
developing world = TB and sarcoidosis
Secondary
Iatrogenic - suppression of the HPG axis - steroids
other causes can be adrenal mets (liver, lung, breast) and adrenal haemorrhage

195
Q

what is the short synacthen test

A

it tests the adrenal reserve:
1. measure basal cortisol at 9am (normally highest here)
2. Administer synacthen
3. sample cortisol again after 30 minutes
if plasma cortisol is above 580nmol/L after 30 minutes then exclude Addison’s

196
Q

what is an adrenal crisis

A

a severe adrenal insufficiency especially hypocortisolemia, with nausea and vomiting, renal failure, LOC

197
Q

what is the treatment for adrenal crisis

A

immediate hydrocortisone and IV solute and dextrose if they are hypoglycaemic

198
Q

what is the gold standard test for acromegaly

A

an impaired glucose tolerance

199
Q

what are complications of acromegaly

A

type 2 diabetes malitis and sleep apnoea

200
Q

what are the two types of diabetes insipidus

A

cranial (reduced ADH secretion) and nephrogenic (reduced kidney response to ADH)

201
Q

what are examples of pituitary mass lesions

A

-non functioning pituitary adenomas
-endocrine active pituitary adenomas
-malignant pituitary tumours; functional and non functional pituitary carcinomas
-metastases in the pituitary (breast, lung, stomach, kidney)
-pituitary cysts; Rathke’s cleft cyst

202
Q

what is a craniopharyngioma

A

arises from squamous epithelial remnants of Rathke’s pouch
- tumour infiltrates the surrounding structures and can cause visual disturbance, growth failure, and pituitary hormone deficiency.

203
Q

what is Rathkes pouch

A

it is an evagination at the roof of the developing mouth in front of the buccopharyngeal membrane which gives rise to the anterior pituitary.

204
Q

what is a Rathke’s cyst

A

it is derived from the remnants of the pouch and is mostly asymptomatic and small. However it can present with headache and amenorrhoea, hypopituitarism and hydrocephalus

205
Q

what is a meningioma

A

it is a tumour of the meninges and can often be caused by radiotherapy
- causes loss of visual acuity, endocrine dysfunction and visual field defects

206
Q

What are the symptoms of a non functioning pituitary adenoma

A

if its large it can cause signs of aggressiveness, and mood changes, with 50% causing visual disturbance and 50% causing headaches

207
Q

how do you treat a non functional tumour

A

you would do a trans-sphenoidal surgery if its threatening the patients eyesite, or if its increasing in size

208
Q

what is a non functioning pituitary adenoma

A

They are pituitary tumour masses which don’t produce and hormones - account for about 10-15% of primary intracranial tumours

209
Q

how would you test pituitary function

A
  • test hormone function: GH, LH/FSH, ACTH, TSH, ADH
  • look at circadian rhythms and pulsatile release of hormones
  • look at how the peripheral target organ is working
210
Q

what are consequences of growth hormone deficiency

A

short stature
abnormal body composition
reduced muscle mass
poor quality of life

211
Q

what are consequences of LH/FSH deficiency

A

hypogonadism
reduced sperm count
infertility
menstruations problems

212
Q

how do you treat LH/FSH disorders

A

testosterone in males
oestradiol and progesterone in females

213
Q

what are consequences of TSH deficiency

A

hypothyroidism

214
Q

how do you treat TSH disorders

A

levothyroxine

215
Q

what are consequences of ACTH deficiency

A

adrenal failure
decreased pigment

216
Q

how do you treat ACTH deficiency

A

Give corticosteroids such as hydrocortisone

217
Q

What are consequences of ADH deficiency

A

diabetes insipidus, decreased water absorption in the kidney resulting in polyuria and polydipsia

218
Q

how do you treat ADH deficiency

A

DDAVP - desmopressin

219
Q

how much water is in the extracellular fluid

A

1/3 of total body water - 14L

220
Q

how much water is found in the
a. intravascular fluid
b. interstitial fluid

A

a. 3.5L (1/4 of ECF)
b. 10.5L (3/4 ECF)

221
Q

how much water is in the intracellular fluid

A

28L - 2/3 of total body water

222
Q

what occurs physiologically when youre in water excess

A

there is a decrease in plasma osmolality causing an increase in cellular hydration. There is a reduction in thirst, and therefore reduced water intake. You also have a reduction in vasopressin secretion, causing an increase in urine water excretion by the kidney. this and the lack of thirst will reduce total body water

223
Q

what occurs physiologically when you are in water deficit

A

water loss causes an increase in plasma osmolality and therefore a decrease in cellular hydration. This will activate the thirst reflex to increase water intake, as well as increasing vasopressin secretion thus reducing water excretion by the kidney. These two things will increase total body water

224
Q

what is the release of vasopressin controlled by

A
  • osmoreceptors
  • baroreceptors
225
Q

where are osmoreceptors found

A

in the hypothalamus

226
Q

where are baroreceptors found

A

found in the brainstem and in the great vessels

227
Q

what is the osmolality

A

concentration per kilo

228
Q

what are some of the causes of cranial diabetes insipidus

A

things that cause a lack of vasopressin
- idiopathic
- trauma
- tumours
- genetic
- vascular - aneurysms or infarction

229
Q

how do you manage cranial diabetes insipidus

A

you would treat any underlying condition
use desmopressin

230
Q

when is someone hyponatraemic

A

when their serum sodium is less than 135mmol/L

231
Q

what is the normal serum sodium range

A

137-144mmol/L

232
Q

what are the signs and symptoms of hyponatraemia

A

headache
lethargy
anorexia
abdominal pain
weakness
confusion and hallucinations

233
Q

what tests would someone get done when suspected to be hyponatraemic

A

plasma osmolality
urine osmolality
plasma glucose
urine sodium
cortisol

234
Q

what is the indicator of the start of puberty in
a. men
b. women

A

a. first ejaculation - often nocturnal
b. menarche - first period

235
Q

what causes development in secondary sexual characteristics in women

A

ovarian oestogens regulate the growth of breast and female genitalia. Ovarian and adrenal androgens control puberty and axillary hair

236
Q

what causes development of secondary sex characteristics in males

A

testicular androgens cause external genitalia and pubic hair growth and enlargement of the larynx and laryngeal muscles (voice deepening)

237
Q

what are the tanner stages

A

it is a scale that defines physical measurements of development based on external primary and secondary sexual characteristics

238
Q

what is thelarche

A

it is breast development - first visible change of puberty

239
Q

what is thelarche induced by

A

oestrogen increase

240
Q

how long does it take to complete thelarche

A

completed in about 3 years

241
Q

what are the effects of oestrogen on the breast

A
  • ductal proliferation
  • site specific adipose deposition
  • enlargement of the areola and nipple
242
Q

what other hormones are involved in breast development

A

prolactin, glucocorticoids and insulin

243
Q

what is precocious puberty

A

it is early onset of secondary sexual characteristics, before 8 years in girls and before 9 in boys

244
Q

what can menarche before 9 lead to

A

short stature

245
Q

what is delayed puberty

A

the absence of secondary sexual characteristics by 14 years (girls) and 16 years (boys)

246
Q

what does delayed puberty lead to

A

can lead to reduced peak bone mass and osteoperosis

247
Q

what is adrenarche

A

it is the maturational process of the adrenal gland which causes a mild advance in bone age, axillary hair, oily skin, mild ache and body odour

248
Q

what is pubarche

A

it is the most pronounced clinical result of adrenarche

249
Q

in girls what calls for investigations of delayed puberty

A
  1. lack of breast development
  2. over five years between breast development and menarche
  3. lack of pubic hair by aged 14yrs
  4. absent menarche by age 15-16yrs
250
Q

in boys what calls for investigations of delayed puberty

A
  1. lack of testicular enlargement by age 14yrs
  2. lack of pubic hair by age 15
  3. more than 5 years to complete genital enlargement
251
Q

what lab investigations are done when delayed puberty is suspected

A
  1. complete red blood count
  2. U+E, renal, LFT
  3. LH and FSH
  4. testosterone/oestradiol
  5. thyroid function
  6. prolactin
252
Q

what may be some functional causes as to why someone has delayed puberty

A
  1. chronic renal disease
  2. chronic lung disease
  3. anorexia nervosa
  4. psychological/stress related problems
  5. drugs
253
Q

what is primary hypogonadism

A

when there is a problem at the ovary or testis which causes a reduction or complete absence in hormone secretion from the glands

254
Q

what is secondary hypogonadism

A

this is where the issue is at the pituitary or hypothalamus, aka, no LH/FSH or GnRH

255
Q

what happens in primary female hypogonadism

A

oestrogen decreases which causes a lack of negative feedback, this causes a rise in LH and FSH (seen on blood)

256
Q

what happens in secondary female hypogonadism

A

there is low/no LH or FSH release meaning there is no response to feedback. Therefore oestrogen decreases

257
Q

what happens in primary male hypogonadism

A

testosterone release is low or not there. therefore there is lack of feedback. Therefore there is LH and FSH increase

258
Q

what happens in secondary male hypogonadism

A

LH and FSH are low/not made and therefore there is no response to feedback meaning testosterone also decreases

259
Q

what is turners syndrome

A

45 X0 in girls

260
Q

what are symptoms of turners syndrome

A
  • renal malformations; horseshoe kidney (fusion)
  • short stature
  • cardiovascular malformations: aortic arch, spontaneous rupture
261
Q

how common is turner syndrome

A

occurs in 1 in 2000 girls

262
Q

what are different causes of thyroid autoimmunity

A
  • postpartum thyroiditis
  • autoimmune thyroiditis
  • autoimmune hypothyroidism
  • graves disease
263
Q

what is found in almost all patients with autoimmune hypothyroidism

A

thyroglobulin and thyroid peroxidase (TPO) antibodies

264
Q

what can predispose you to hypothyroidism

A
  • genetic and environmental factors in varying proportion
  • being female
  • environmental factors; stress, high iodine intake, smoking
265
Q

what is a goitre

A

it is a palpable and visible thyroid enlargement

266
Q

where are goitres endemic

A

in iodine deficient areas

267
Q

what is the definition of hyperthyroidism

A

an excess of thyroid hormone in the blood

268
Q

what are the three main mechanisms for increased levels of thyroid hormone in the body

A
  1. overproduction of thyroid hormone
  2. leakage of preformed hormone from the thyroid
  3. ingestion of excess thyroid hormone
269
Q

what are causes of hyperthyroidism

A
  • graves disease
  • toxic multinodular goitre
  • toxic adenoma
  • congenital hyperthyroidism
  • thyroiditis
  • iodine induced
270
Q

what are the clinical features of hyperthyroidism

A
271
Q

What is an adenoma specific symptom for hyperthyroidism

A

a solitary nodule

272
Q

what is a MNG specific symptom for hyperthyroidism

A

multinodular goitre

273
Q

what investigations are done to diagnose hyperthyroidism

A
  1. thyroid function tests to confirm biochemical hyperthyroidism
  2. diagnosis of the underlying cause cause its important to treat
  3. clinical history, physical signs
  4. supporting investigations, such as thyroid antibodies
274
Q

what are the three tyes of hypothyroidism

A

primary, secondary, tertiary
- primary is 99% of cases where there is absence or dysfunction to the thyroid gland

275
Q

what is a common cause of primary hypothyroidism

A

hashimotos thyroiditis

276
Q

what are causes of hypothyroidism in a child

A
  • neonatal hypothyroidism
  • resistance to thyroid hormone
  • isolated TSH deficiency
277
Q

what drugs can cause hypothyroidism

A

iodine, lithium and thionamides

278
Q

what are the actions of the parathyroid hormone

A
  1. increases calcium reabsorption in the kidney
  2. increases 1 alpha hydroxylation of 25-OH vitamin D in the kidney
  3. decreases phosphate reabsorption in the kidney
  4. increases bone remodeling (bone resorption greater than formation)
  5. indirectly increases calcium reabsorption in the intestine
279
Q

what is hypocalcaemia

A

low total serum calcium

280
Q

what are the consequences of hypocalcaemia

A

paraethesia - burning or prickling sensation in hands, legs, arms and feet
muscle spasm
seizures
basal ganglia calcification
cataracts
ECG abnormalities
Osteomalacia - vitamin D deficiency

281
Q

what is the calculation for working out the corrected calcium

A

the total serum calcium + 0.02

282
Q

what is Chvostek’s sign

A

when you tap over the facial nerve and look for spasm of the facial muscles

283
Q

what is hypoparathyroidism

A

it is the underproduction of the parathyroid hormone

284
Q

what are causes of hypoparathyroidism

A
  1. genetics
  2. autoimmune - isolated, polyglandular
  3. infiltration of the parathyroid glands by iron overload (haemochromotosis)
  4. surgery - parathyroidectomy
285
Q

what is pseudohypoparathyroidism

A

resistance to parathyroid hormone

286
Q

what would the bloodwork show in someone who had pseudohypoparathyroidism

A

low serum calcium and high phosphate, but appropriate PTH levels for the low calcium levels

287
Q

what are the consequences of pseudohypothyroidism

A

short stature
obesity
round faces
mild learning difficulties
short fourth metacarpals
other hormone resistance

288
Q

what is hypercalcaemia

A

high calcium levels in the blood serum - >2.66 mmol/L

289
Q

leaving what on for too long can cause hypercalcaemia

A

leaving a tourniquet on for too long

290
Q

what are some symptoms of hypercalcaemia

A

thirst
polyuria
nausea
constipation
confusion
can lead to coma
painful bones
renal stones
GI symptoms
Psychosis
vomiting
cardiac arrest

291
Q

what can hypercalcaemia be a consequence of

A

Calcium supplementation
Hyperparathyroidism
Iatrogenic drugs – thiazides
Milk alkali syndrome
Paget’s disease of bone
Acromegaly and Addison’s
Zolinger-Ellison Syndrome – MEN type I
Excess vitamin D
Excess vitamin A
Sarcoidosis

292
Q

what is primary hyperparathyroisism

A

it is increased PTH levels due to a problem with the parathyroid glands - often a tumour
- 80% solitary adenoma
- 20% hyperplasia of glands

293
Q

what are consequences of primary pyerparathyroidism

A

bones - osteitis fibrosa cystica, osteoperosis
kidney stones
psychic groans - confusion
abdominal moans - constipation and acute pancreatitis

294
Q

what happens to PTH, calcium and phosphate levels in vitamine D deficiency

A

PTH - High
Calcium - Low
Phosphate - Low

295
Q

Is the response of phosphate in vitamin D deficiency appropriate or not

A

it is appropriate

296
Q

what happens to PHT, calcium and phosphate levels in hypoparathyroidism

A

PTH - low - inappropriate
Calcium - Low
Phosphate - high

297
Q

what happens to PTH, calcium and phosphate in pseudohypoparathyroidism

A

PTH - High - appropriate
Calcium - low
Phosphate - high

298
Q

what happens to PTH, calcium and phosphate during hypercalcaemia of malignancy

A

PTH - low - appropriate
calcium - high
Phosphate - unpredictable, depends on underlying cause

299
Q

What is SIADH

A

syndrome of inappropriate ADH: large amounts secreted causing water to be reabsorbed in the collecting duct

300
Q

what are causes of SIADH

A
  • post operative from major surgery
  • infection (atypical pneumonia and lung abscess)
  • head injury
  • medication (thiazide diuretics, carbamazepine, antipsychotics, SSRIs, NSAIDs)
301
Q

what are signs and symptoms of SIADH

A

headache
nausea
fatigue
muscle cramps
confusion
severe hyponatraemia

302
Q

what investigations need to be done with SIADH

A

is a diagnosis of exclusion
- look for U and E - hyponatraemia
- Urine sodium is high
- urine osmolality is high

303
Q

what causes of hyponatraemia need to be excluded

A

do a negative short synACTHen test - exclusive adrenal insufficiency
no diarrhoea and vomiting
no history of diuretic use
no AKI/CKD

304
Q

how do you manage SIADH

A

treat the underlying cause:
stop the causative medicine
fluid restriction
Tolvaptan (ADH receptor blocker)

305
Q

when is someone considered hyperkalaemic

A

when their level is above 5.5mmol/L

306
Q

what are the symptoms of hyperkalaemia

A

fatigue and light headedness
weakness
chest pain
palpitations

307
Q

what are the symptoms of hyperkalaemia

A

arrhythmias - potential for cardiac arrest
reduced power and reflexes
flaccid paralysis
signs of underlying cause

308
Q

what are the different causes of hyperkalaemia

A

Due to excessive consumption at a fast rate - IV fluids
Low levels of aldosterone in kidneys – adrenal insufficiency (addisons disease)
Drugs - ACE inhibitors, Spironolactone – potassium-sparing diuretic
NSAIDs, Ciclosporin, Heparin
Acute kidney injury – decreased filtration rate so more K+ is maintained in blood

309
Q

what will happen on a ECG when someone is hyperkalaemic

A

there will be a small of even absent P wave. There will be prolonged PR intervals and a wide QRS interval (over 0.12s) . There will also be Tall tented T waves
- may not all be present

310
Q

what investigations will be done if someone is suspected of having hyperkalaemia

A
  • ECG
  • Bloods - FBC and U+E
  • Urine osmolality and electrolytes
311
Q

how do you treat hyperkalaemia

A

ABC - Urgent care
Cardiac monitoring
Calcium gluconate - to protect myocardium
Insulin and dextrose or nebulised salbutamol to drive up potassium intracellularly
treat the underlying cause

312
Q

when is someone hypokalaemic

A

when they have less than 3.5mmol/L in the blood

313
Q

what are symptoms of hypokalamia

A
  • can be asymptomatic
  • fatigue and lightheadedness
  • weakness
  • cramps
  • palpitations
  • constipation
314
Q

what are signs of hypokalaemia

A
  • arrhythmia
  • hypotonia
  • hyporeflexia
  • muscle paralysis
  • rhabdomyolysis
  • constipation
315
Q

what are reasons why someone would get hypokalaemia

A

increased excretion - renal disease, drug effect (thiazides, loop diuretics, laxatives), GI loss (D+V), Conns syndrome, Cushings
decreased intake; Dietary deficiency or fasting, liquorice abuse
shift to intracellular; metabolic alkalosis, drug effects (insulin, B2 agonists)
GI losses - vomiting, severe diarrhoea and laxative abuse

316
Q

what would you see on an EGC in hypokalaemia

A

a prolonged PR interval, ST depression, flat T waves, long QT, and prominent U waves

317
Q

what investigations are done when someone is suspected of having hypokalaemia

A
  • ECG
  • Bloods - FBC and U+E
  • urine osmolality and electrolytes
318
Q

what treatments would you give someone with hypokalaemia

A

potassium - PO/IV
other electrolytes as requires
treat underlying cause
MILD: Usually asymptomatic (3.0-3.4mmol/L)
Oral replacement- consider IV
SEVERE: <2.5mmol/L
- IV replacement 40mmol KCL in 1L 0.9 NaCl

319
Q

what are the two types of diabetes insipidus

A

cranial and nephrogenic

320
Q

what is the pathophysiology of diabetes insipidus

A
  • impaired water resorption
  • large volumes of dilute urine
321
Q

what are the reasons for cranial diabetes insipidus

A

idiopathic
congenital
tumour
trauma
infection

322
Q

what are nephrogenic causes of diabetes insipidus

A

inherited
metabolic - low potassium and high calcium
drugs - lithium
- chronic renal disease

323
Q

what is the gold standard test for diabetes insipidus

A

the 8 hour water deprivation test

324
Q

how do you treat
a. nephrogenic
b. cranial diabetes insipidus

A

a. if it persists give bendroflumethiazide
b. desmopressin

325
Q

what are the causes of a. primary, b. secondary and c. tertiary causes of hyperparathyroidism

A

a. parathyroid gland produces excess PTH
b. increased secretion of PTH to compensate hypocalacemia
c. autonomous secretion even after correction of calcium deficiency due to chronic kidney disease

326
Q

what investigations are done for hyperparathyroidism

A

PTH/bone profile: high PTH, high calcium and low phosphates
primary: raised calcium
secondary: low serum calcium, high PTH
tertiary: raised calcium and raised PTH

DEXA scan, X ray, ultrasound for stones

327
Q

how do you manage hyperparathyroidism

A

primary; sergical removal or adenoma, give bisphosphonates
secondary; calcium correction, treat underlying cause
tertiary; cinacelcet (calcium mimetic) and total/part parathyroidectomy

328
Q

what can cause a. primary and b. secondary hypoparathyroidism

A

a. primary - gland failure - autoimmune destruction, congenital (DiGeorge syndrome)
b. Secondary - surgical removal, decreased magnesium (needed for PTH secretion)

329
Q

what is Trousseaus’s sign

A

it is where BP cuff causes wrist flexion and the fingers to pull together

330
Q

what investigations are done in hypoparathyroidism

A

bloods - bone profile, decreased calcium, increased or normal phosphate, decreased PTH
ECG - prolonged QT +ST segments

331
Q

how do you treat hypoparathyroidism

A

IV calcium
AdCal D3 - calcitriol
synthetic PTH if they require it

332
Q

what age does type 1 diabetes mellitus usually begin

A

usually between the ages of 5-15

333
Q

what is the pathophysiology of type 1 diabetes mellitus

A
  1. autoimmune destruction of beta cells in the islets of langerhans by autoantibodies
  2. insulin deficiency and continued breakdown of liver glycogen
  3. hyperglycaemia and glycosuria
334
Q

what is the pathophysiology of diabetic ketoacidosis

A
  1. complete absence of insulin leads to unrestrained increased hepatic gluconeogenesis and decreased peripheral glucose uptake
  2. this leads to hyperglycaemia and therefore osmotic diuresis and dehydration
  3. there is peripheral lipolysis to gain more glucose and free fatty acids increase and are oxidies into ketones causing a build up and leading to acidosis
335
Q

what factors increase the risk of type 2 diabetes

A

increases with age
male over female
ethnicity; African-carribean, black African and south Asian
obesity
hypertension

336
Q

what is the mechanism of action of metformin

A

it decreases gluconeogenesis in the liver and increases cell sensitivity to insulin

337
Q

what is the mode of action of sulfonylureas

A

promotes insulin secretion from the beta cels

338
Q

what investigations are done to diagnose Conns syndrome

A

plasma potassium - low
aldosterone/renin ratio - high

339
Q

what is a phaeochromocytoma

A

an adrenal medullary tumour that secretes catecholamines

340
Q

what are signs symptoms of phaeochromocytomas

A

Signs; hypertension, postural hypotension, tremor, hypertensive retinopathy, pallor
symptoms; headache, sweating, palpitations, tremor

341
Q

what investigations are done for phaeochromocytomas

A

plasma metanephrines and normetanephrines
24 hour urinary total catecholamines
CT

342
Q

what is the treatment for phaeochromocytomas

A

1st line; alpha blockers; phenoxybenzamine
without a HTN crisis
1st line; Antihypertensive agents; phentolamine
with HTN crisis

343
Q

what is carcinoid syndrome

A

a group of syndromes due to the release of serotonin and other vasoactive peptides into the systemic circulation from a tumour.

344
Q

what are the signs and symptoms of carcinoid syndrome

A

signs; palpitations, abdominal cramps, signs of right sided heart failure, bronchospasm
symptoms; diarrhoea and flushing

345
Q

what investigations are done to diagnose carcinoid syndrome

A

high volume of 5 hydroxyindoleactic acid (breakdown product)
metabolic panel and LFTs
liver ultrasound

346
Q

what is the treatment for carcinoid syndrome

A
  1. local disease: surgical resection and peri-operative octreotide infusion
  2. metastasis; above plus additional radio ablation
347
Q

what does Conn’s syndrome refer to

A

PRIMARY aldosterone producing adenoma

348
Q

what are causes of Conn’s syndrome

A

2/3 cases; solitary aldosterone producing adrenal adenoma
1/3 cases; bilateral adrenocortical hyperplasia (technically not conns)

349
Q

what is the pathology of conns syndrome

A

excess production of aldosterone, independent of RAAS
- increases K+ loss, Na+ and water retention causing a raised BP
- decreased renin release
- Hypokalaemia

350
Q

what are symptoms of Conns syndrome

A

it is usually asymptomatic
- constipation
- muscle weakness and cramps
- polyuria and polydipsia
- paraesthesia
unusual symptoms - sweating attacks

351
Q

what are signs of conns syndrome

A

hypertension due to increased blood volume
increased risk of cardiac arrhythmias, particularly in patients with cardiac disease

352
Q

what are differential diagnosis of conns disease

A

secondary hyperaldosteronism - excess renin

353
Q

what does hypokalemia look like on an ECG

A

slightly peaked P waves
Slightly prolonged PR interval
ST depression
Shallow T wave
Prominent U wave

354
Q

what are investigations done for conns syndrome

A

U&Es - decreased renin and increased aldosterone
EGC
Adrenal CT/MRI - aldosterone producing adenoma

355
Q

What is the pathology of SIADH

A

Excess ADH causes an increase in AQP2 insertion, and therefore increased water retention and dilution of plasma (hyponatraemia)
BUT ALSO
Excess ADH causes increased insertion of AQP2 increasing water retention and therefore preventing RAAS release. Therefore there is secretion of Na+ and excess water removed with the Na+ so you are euvolaemic but HYPONATEAEMIC

356
Q

what are malignant causes of SIADH

A

disordered hypothalamic pituitary secretion or ectopic production
malignancy - small cell lung carcinoma, prostate, thymus, pancreas

357
Q

what are drug causes of SIADH

A

Drugs - opiates, chlorpropamide, carbamazepine, vincristine

358
Q

what are brain causes of SIADH

A

brain - meningitis, cerebral abscess, head injury, tumour

359
Q

what are lung causes of SIADH

A

lung - pneumonia, TB, abscesses, asthma, CF

360
Q

what are metabolic causes of SIADH

A

Metabolic - porphyria and alcohol withdrawal

361
Q

what are symptoms of SIADH

A

reduction in GCS and confusion with drowsiness
irritability
headaches
anorexia
nausea

362
Q

what is the treatment for SIADH

A

treat the underlying cause
Restrict fluid - to increase Na+ concentration
Demeclocycline - inhibits action of vasopressin on the kidney
Vasopressin receptor antagonists
Tolvaptan - promotes water excretion with no loss of electrolytes
furosemide (oral)

363
Q

what is Kussmaul’s respiration

A

low, deep, sighing/laboured inspiration

364
Q

What is the pathology of hyperkalaemia

A

When K+ levels in blood rise, this reduces the different in electrical potential between cardiac myocytes and outside of the cells. this causes the threshold for action potentials to be significantly decreased and therefore abnormal action potentials occur, causing arrhythmia and cardiac arrest

365
Q

what is the pathology of hypokalaemia

A

low serum potassium causes a cater concentration gradient out of the cell. This increases leakage from the intracellular fluid causing hyperpolarisation of the myocyte membrane and decreasing myocyte excitability

366
Q

what happens on an ECG when calcium is too high

A

the QT interval gets shorter

367
Q

what happens on an ECG when calcium is low

A

the QT interval gets longer

368
Q

what are the causes of hypocalcaemia

A

vitamin D deficiency - presents with low phosphate
hypoparathyroidism - presents with high phosphate
acute pancreatitis - presents with low phosphate
osteomalacia - presents with low phosphate
chronic kidney disease - presents with high phosphate
pseudohypoparathyroidism
drugs - calcitonin and bisphosphonates

369
Q

what is osteomalacia

A

soft bones due to low serum calcium and vitamin D deficiency
- serum calcium low as calcium cant be absorbed from the blood, parathyroid responds to this and makes PTH to suck calcium from kidneys and resorb bone

370
Q

what is chvosteks sign used for

A

testing low serum calcium

371
Q

what is trousseaus sign used for

A

testing low serum calcium

372
Q

what is the treatment for hypocalcaemia

A

Mild – Adcal supplement (calcium carbonate) or cholecalciferol
Severe – Calcium gluconate
Vitamin D supplementation in persistent hypocalcaemia

373
Q

what are investigations done for hypercalcaemia

A

ECG - short QT
CXR - rule out myeloma and lymphoma
24 hour urinary calcium
bloods - calcium and PTH
X-ray and protein electrophoresis
DEXA bone scan
high resolution CT
TSH to exclude hyperthyroidism
Tetracosactide to exclude Addisons

374
Q

what is the treatment for hypercalcaemia

A

Lowering calcium levels and treatment of underlying cause
Primary hyperparathyroidism – surgical removal of symptomatic parathyroid adenoma
IV saline – helps to dilute levels of calcium in blood
Bisphosphonates – encourage osteoclasts to undergo apoptosis so there is less bone breakdown

375
Q

what inhibits the release of growth hormone

A

Somatostatin
High levels of glucose
Dopamine (not as potent as somatostatin)

376
Q

what is the definition of diabetes mellitus

A

a group of chronic disorders characterised by the bodies impaired ability to produce or respond to insulin resulting in abnormal glucose metabolism leading to hyperglycaemia

377
Q

A three year old boy with a history of type 1 diabetes presents to A&E with vomiting and lethargy. On examination he is dehydrated. Bloods gas and ketones are done and its confirmed he has moderate diabetic ketoacidosis. What treatment should be commenced first?

A

IV 0.9% sodium chloride

378
Q

what is the presentation of diabetic ketoacidosis

A

Nausea and vomiting
Dehydration (hypotension)
Acetone smelling breath
Abdominal pain
Drowsy or confused which can progress to coma
reduced consciousness
Hyperventilation (Kussmaul breathing)

379
Q

What is the gold standard test for diagnosing type 2 diabetes

A

the HbA1c test - tells you average blood glucose over three months

380
Q

what does some ones HbA1c test have to be for them to be diagnosed with pre-diabetes

A

42-47mmol/L

381
Q

what are the microvascular complications of diabetes mellitus

A

nephropathy
retinopathy
peripheral neuropathy

382
Q

what are the macrovascular complications of diabetes mellitus

A

stroke
hypertension
coronary artery disease
peripheral artery disease

383
Q

what are the main side effects of metformin

A

Gastrointestinal upset
lactic acidosis

384
Q

what are the main side effects of sulfonylureas

A

hypoglycaemia
weight gain
hyponatraemia

385
Q

what are side effects of DPP-4 inhibitors

A

generally well tolerated but increased risk of pancreatitis

386
Q

what are the main side effects of GLP-1 agonists

A

Nausea and vomiting
pancreatitis

387
Q

what drug class is metformin a part of

A

Biguanides

388
Q

what is the pathophysiology of hyperosmolar hyperglycemic state

A

decreased insulin levels are sufficient to inhibit hepatic ketogenesis (because its not absolute insulin deficiency) but insufficient to inhibit hepatic glucose production. This leads to hyperglycaemia and therefore osmotic diuresis with loss of sodium and potassium

389
Q

how does hyperosmolar hyperglycemic state present

A

General: Fatigue, lethargy, nausea and vomiting
Neurological: altered level of consciousness with headaches, papilloedema and weakness
Haematological: hyperviscosity
Cardiovascular: dehydration, hypertension, tachycardia

390
Q

how do you diagnose hyperosmolar hyperglycemic state

A

severe hyperglycaemia (>30mmol/L)
hypotension
hyperosmolality
(no significant acidosis or ketosis)

391
Q

what is the treatment of hyperosmolar hyperglycemic state

A

Fluid replacement with 0.9% saline
VTE prophylaxis - these patients are high risk due to dehydration
Give insulin - only if glucose doesn’t decrease after fluid replacement

392
Q

what are complications o hyperosmolar hyperglycemic state

A

Stroke
MI
PE
Insulin related hypoglycaemia
treatment related hypokalaemia

393
Q

A 56-year-old diabetic female is admitted to hospital in order to have intravenous antibiotics for community acquired pneumonia. On day 4 of admission, she becomes confused and drowsy after which she has a short seizure which spontaneously resolves. Her capillary glucose is noted at 2.6mmol/L and she is unconscious.
What is the most appropriate immediate management of this patient?

A

IV glucose

394
Q

what is the definition of hypoglycaemia

A

hypoglycaemia occurs when glucose concentration falls below the normal fasting glucose level, generally this is defined as glucose below 3mmol/L

395
Q

what is the normal body response to hypoglycaemia

A

Blood glucose taken up by cells, levels of glucose within blood drop.
Stimulates alpha islet cells 🡪 produce glucagon and reduce production of insulin from beta cells.
Glucagon acts to increase liver gluconeogenesis and glycogenolysis.

↓ Blood glucose 🡪 increased production of adrenaline, GH and cortisol levels
All these mechanism act to increase blood glucose rapidly.

396
Q

how does hypoglycaemia present when the patient has blood glucose of less than 3.3mmol/L

A

Sweating
shaking
hunger
anxiety
nausea

397
Q

How does hypoglycaemia present when the patient has a blood glucose of less than 2.3mmol/L

A

weakness
vision changes
confusion
dizziness

398
Q

What is the pathophysiology behind primary hypothyroidism

A

Problem at the thyroid level causing low T3/4 being produced
There will be compensatory high TSH levels but due to thyroid dysfunction it doesnt increase T3/4 levels

399
Q

what is the pathophysiology behind secondary hypothyroidism

A

Pituitary disorders cause low levels of TSH and therefore low T3/4

400
Q

what other tests are done for hypothyroidism (other than TFT and antibody test)

A

Fasting blood glucose - recommended in assessment in patients with non specific fatigue and weight gain (primary hypothyroidism is associated with type 1 diabetes)

401
Q

what is Hashimoto’s thyroiditis

A

An autoimmune disease causing the thyroid to be attached by an immune mediated processes

402
Q

what is the pathophysiology of hashimotos

A

The pathophysiology of Hashimoto thyroiditis involves the formation of antithyroid antibodies that attack the thyroid tissue, causing progressive fibrosis. (Low T4 and High TSH).
Associated with type 1 diabetes mellitus, Addison’s or pernicious anaemia and may cause transient thyrotoxicosis in the acute phase

403
Q

what investigations are done for hashimotos

A

1ST LINE = Thyroid function tests(TFTs)- Primarily look at TSH ad T4 levels (Low T4 and High TSH)
GS = Antithyroid peroxidase antibodies- POSITIVE

404
Q

what is the treatment for hashimotos

A

same as in hypothyroidism - levothyroxine

405
Q

what investigations are done to diagnose graves

A

Thyroid function tests(TFTs)- Primarily look at TSH ad T4 levels (High T4 and low TSH)
TPO-Ab, Isotope scan, MRI, CT, Ultrasound

406
Q

what is the treatment for graves disease

A

Anti-Thyroid drugs- block thyroid hormone synthesis, carbimazole, thiamazole
Radioactive iodine therapy-
Surgery
Patients with active moderate to severe and sight-threatening orbitopathy first-line treatment is intravenous corticosteroid (e.g., methylprednisolone)

407
Q

What is De Quervain’s thyroiditis

A

De Quervain’s (subacute) thyroiditis is a painful swelling of the thyroid gland thought to be triggered by a viral infection, such as mumps or flu.
- rapid swelling or the thyroid

408
Q

what is the pathophysiology of De Quervains’s thyroiditis

A

There are typically 4 phases:
Phase 1- lasts 3-6 weeks: hyperthyroidism, painful goitre, Raised ESR
Phase 2- Lats 1-3 weeks: Euthyroid (normal function)
Phase 3- weeks to months: Hypothyroidism
Phase 4- Thyroid structure and function goes back to normal

409
Q

how does De Quervains thyroiditis present

A

Neck pain, difficulty eating, tender, firm, enlarged thyroid, fever, palpitations

410
Q

what is diagnosis/investigations done for De Quervains thyroiditis

A

Total T4, 3 levels
T3 resin uptake
free thyroxine index
all elevated

411
Q

what is the treatment of De quervains

A

Hyperthyroid phase - NSAIDS and corticosteroids can be used for pain
Hypothyroid phase - No treatment normally but can give small dose of levothyroxine in severe cases.

412
Q

what are complications of de quervains thyroiditis

A

thyroid storm, long term hypothyroiditis

413
Q

what are the four types of thyroid cancer

A

papillary, follicular, anaplastic, medullary

414
Q

what are causes for thyroid cancer

A

genetic alteration and mutations
head and neck irradiation
female sex

415
Q

how does thyroid cancer present

A

palpable thyroid nodule

416
Q

who do you diagnose thyroid cancer

A

US neck - fine needle biopsy
laryngoscopy

417
Q

how do you treat thyroid cancer

A

thyroidectomy followed by radioactive iodine ablation and suppression of TSH

418
Q

what are complications of thyroid cancer

A

Complications of total thyroidectomy include an increased risk of recurrent laryngeal nerve damage or hypoparathyroidism

419
Q

what is the definition of a thyroid storm

A

Thyroid storm (also known as thyroid or thyrotoxic crisis) represents the severe end of the spectrum of thyrotoxicosis and is characterized by compromised organ function (Rare)

420
Q

what are causes of thyroid storm

A

Graves disease, Post thyroidectomy, Infection, Trauma, MI, DKA, Pregnancy etc, Exogenous iodine, Abrupt cessation/Lack of adherence with Antithyroid drugs

421
Q

what is the presentation of a thyroid storm

A

Fever, cardiovascular dysfunction, profuse sweating, tachyarrhythmias, nausea and vomiting

422
Q

what is the pathophysiology of acromegaly

A

GHRH is released from the hypothalamus and stimulates the release of GH from the anterior pituitary.
The excess growth hormone (GH) from the anterior pituitary results in excessive production of insulin like growth factor (IGF-1) which is responsible for inappropriate growth. This stimulates bone and soft tissue growth.

423
Q

how do you treat acromegaly

A

Trans-sphenoidal surgery of the pituitary tumour is gold standard tx for acromegaly secondary to pituitary adenomas.
Surgical removal of cancer is tx for acromegaly secondary to cancer.
If the above don’t work there are medication that can be used to block GH.
2nd line-Somatostatin analogues to block GH release (e.g. octreotide)
3rd line- Pegvisomant (GH antagonist given subcutaneously and daily) OR
Dopamine agonists to block GH release (e.g. bromocriptine)

424
Q

what are complications of acromegaly

A

Type 2 diabetes - due to constant high glucose levels
Heart disease- due to possible hypertrophy of the heart due to increased GH
Hypertension
Arthritis - due to overgrowth of cartilage
Carpal tunnel - as muscle growth compresses nerves
Visual fields defect- Bitemporal Hemianopia

425
Q

what is prolactin

A

It is a hormone made by lactotrophs in the anterior pituitary and causes breasts to grow and milk made during pregnancy

426
Q

what is the pathophysiology of a prolactinoma

A

Hypersecretion of prolactin causes secondary hypogonadism (hypogonadism caused by a problem in the pituitary or hypothalamus) this is due its inhibitory effects on gonadotrophin-releasing hormone.
Hypogonadism is when sex glands called gonads produce little, if any, sex hormones.

427
Q

what are complications of prolactinomas

A

Infertility, sight loss, raised intracranial pressure due to adenoma growth in the brain.

428
Q

what type of corticoid is aldosterone

A

a mineralcorticoid

429
Q

where does aldosterone act in the kidney

A

Distal tubule to increase sodium absorption and potassium secretion

430
Q

What is secondary hyperaldosteronism

A

Secondary hyperaldosteronism is where excessive renin stimulating the adrenal glands to produce more aldosterone. Serum renin will be high.

431
Q

what is the presentation of adrenal insufficiency

A

Non specific symptoms- Fatigue, Weight loss, Nausea, Vomiting, Hypotension, Abdominal pain
Key symptom- Hyperpigmentation especially in the palmar creases for Addison’s

432
Q

what is the gold standard test for adrenal insufficiency

A

GOLD STANDARD- Short synacthen
Ideally performed in the morning when the adrenal glands are the most “fresh”.
Give patient synacthen (synthetic ACTH).
Blood cortisol is measured at baseline, 30 and 60 minutes after administration.
In healthy patients should stimulate adrenal glands to produce cortisol.
The cortisol level should at least double in response to synacthen.
A failure of cortisol to rise (less than double the baseline) indicates primary adrenal insufficiency

433
Q

what is the pathophysiology of SIADH

A

ADH is produced in the hypothalamus and secreted by the posterior pituitary gland. It stimulates water reabsorption from the collecting ducts in the kidneys.
Excessive ADH results in excessive water reabsorption in the collecting ducts. This water dilutes the sodium in the blood so you end up with a low sodium concentration (hyponatraemia). The water reabsorption is not usually significant enough to cause a fluid overload, therefore you end up with a “euvolaemic hyponatraemia”. The urine becomes more concentrated as less water is excreted by the kidneys therefore patients with SIADH have a “high urine osmolality” and “high urine sodium”.

434
Q

what is cranial diabetes insipidus

A

hypothalamus doesnt produce ADH

435
Q

what is nephrogenic diabetes insipidus

A

the collecting ducts of the kidneys dont respond to ADH

436
Q

what is secondary hyperparathyroidism

A

insufficient vitamin D or chronic renal failure leads to low absorption of calcium from the intestines, kidneys and bones causing hypocalcaemia. This causes the Parathyroid gland to release more PTH and becomes hyperplastic to further increase excess PTH secretion.

437
Q

what is tertiary hyperparathyroidism

A

Usually occurs after prolonged secondary hyperparathyroidism
The glands become autonomous, producing excessive PTH even after the cause of hypocalcaemia has been corrected. Don’t respond to negative feedback.
Long-standing kidney disease is the most common cause.

438
Q

what are risk factors for hyperparathyroidism

A

Elderly women
prolonged, severe calcium or vitamin D deficiency

439
Q

in primary hyperparathyroidism what are the levels of
1. PTH
2. Calcium
3. Phosphate

A
  1. high
  2. high
  3. low
440
Q

in secondary hyperparathyroidism what are the levels of
1. PTH
2. Calcium
3. Phosphate

A
  1. High
  2. Low/normal
  3. depends on underlying cause
441
Q

in tertiary hyperparathyroidism what are the levels of
1. PTH
2. Calcium
3. Phosphate

A
  1. High
  2. High
  3. High
442
Q

how does hyperparathyroidism present

A

It is worth remembering the “renal stones, painful bones, abdominal groans and psychiatric moans” mnemonic for the symptoms of hypercalcaemia:
Painful bones
Renal stones
Abdominal groans refers to symptoms of constipation, nausea and vomiting
Psychiatric moans refers to symptoms of fatigue, depression and psychosis

443
Q

what is the treatment for hyperparathyroidism

A

primary - remove the tumour
secondary - treat Vitamin D deficiency or kidney transplant
tertiary - total or subtotal parathyroidectomy
Calcimimetic - increases sensitivity of parathyroid cells to calcium

444
Q

what are complications of hypocalcaemia

A

Seizure, cardiac arrest (decreases heart rate and contractility)- a medical emergency! Long QT syndrome

445
Q

what are complications of Hypokalaemia

A

Cardiovascular- Chronic heart failure, Acute MI, arrythmias,
Muscle – weakness, depression of deep tendon reflexes, Rhabdomyolysis

446
Q

what is the pathophysiology of carcinoid syndrome

A

Neuroendocrine tumours normally secrete serotonin into the circulation.
With GI tract tumours, hormones secreted> enters enterohepatic circulation> liver inactivates hormones> therefore no symptoms
However, when liver metastases are present (liver tumour)> hormone secretion> released into circulation + liver dysfunction> symptoms.

447
Q

what hormone is released in carcinoid syndrome

A

serotonin

448
Q

what is carcinoid syndrome usually caused by

A

neuroendocrine tumour in the GIT

449
Q

state two symptoms of carcinoid syndrome

A

flushing, diarrhoea, abdominal cramps, bronchospasm, fibrosis

450
Q

what is the definitive treatment for carcinoid syndrome

A

resection of the tumour

451
Q

what is the most common cause of hyperthyroidism and hypothyroidism

A
  1. graves disease
  2. hashimotos disease
452
Q

what is the first line treatment for hypothyroidism

A

levothyroxine

453
Q

what is the antibody most associated with hyperthyroidism

A

Anti TSH receptor

454
Q

A 57-year-old male presents to his GP following several hypoglycaemic episodes. He has a history of type 2 diabetes and heart failure. He is currently being treated with Metformin and Gliclazide
what is the most likely cause of his hypoglycaemic state

A

Gliclazide

455
Q

A 36-year-old female presents to her GP with heat intolerance, sweating and palpitations. She is 10 weeks pregnant but has no other medical history. Bloods tests reveal raised free thyroxine and depressed TSH.

What is the most appropriate initial step to treat this patient’s condition?
Lithium
Carbimazole
Propylthiouracil
Thyroidectomy

A

Propylthiouracil - better in first trimester as its safer for fetus than carbimazole

456
Q

A 50-year-old female presents to her general practitioner with ‘pins and needles’ around her mouth and frequent muscle cramps. On examination, she appears well, however when taking her blood pressure reading, her wrist and fingers began to cramp and flex.

What is the most likely diagnosis?
Hyperkalaemia
Hypocalcaemia
Hypernatraemia
Hypomagnesaemia

A

Hypocalcaemia

Phase 2a - Jemima (11 decks)

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