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Endocrine Flashcards

1
Q

Define diabetes

A

A disorder of carbohydrate metabolism characterised by chronic hyperglycemia due to relative insulin deficiency (type 1) or insulin resistance (type 2)

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2
Q

What is the principal organ of glucose homeostasis

A

Liver

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3
Q

Normal physiological response when need to increase blood glucose (2 processes)

A

Glycogenolysis
Gluconeogenesis
Controlled by glucagon

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4
Q

Main insulin independent tissue

A

Brain

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5
Q

Why is brain the major consumer of glucose

A

Brain function is dependent on a continuous supply as it cannot use free fatty acids for energy as they cannot cross the blood brain barrier

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6
Q

Normal physiological process after feeding

A

Increase in blood glucose 5-10 mins after feeding stimulates insulin secretion and suppresses glucagon
60% of ingested glucose goes to the periphery (muscle) to replenish the glucose store
40% of ingested glucose goes to the liver - glycogenesis

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7
Q

Roles of insulin

A

Decrease hepatic glucose output
Increase glucose uptake into insulin sensitive tissues
Suppresses lipolysis and decreases ketogenesis

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8
Q

Physiology of insulin secretion by the beta cell

A
  1. GLUT-2 glucose transporter has a low affinity for glucose. Glucose flows freely into the beta cell
  2. Glucose is phosphorylated by glucokinase
  3. Increase rate of ATP formation from ADP
  4. Increased ATP concentration closes the K+ channels
  5. Change in membrane polarity
  6. Voltage gated Ca2+ channels open and Ca2+ ions enter the cell
  7. Increased concentration of Ca2+ causes insulin vesicles to move to the outer cell membrane
  8. Insulin is secreted
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9
Q

What form is insulin secreted in

A

Insulin is secreted as proinsulin. Alpha and beta chains are joined together by C peptide. Once proinsulin is secreted C peptide is cleaved off

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10
Q

What is biphasic insulin release

A

First rate response = rapid as it is the release of stored insulin
Second rate response = slower release of newly synthesised insulin

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11
Q

What is the action of insulin in muscle and fat cells

A
  1. Insulin binds to insulin receptor on the muscle/fat cell
  2. The binding activates tyrosine kinase which triggers an intracellular signalling cascade
  3. Insulin mobilises GLUT-4 vesicles in the cell which migrate to the plasma membrane
  4. GLUT-4 vesicles are integrated into the plasma membrane
  5. GLUT-4 vesicles allow glucose to enter the cell
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12
Q

How can you increase GLUT-4 receptors

A

The more glucose there is the more GLUT-4 receptors there are

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13
Q

How can you increase insulin sensitivity

A

Exercise can increase insulin sensitivity

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14
Q

What is type 1 diabetes

A

Inadequate insulin production and secretion by the beta cells of the pancreas caused by autoimmune destruction

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15
Q

Epidemiology of type 1 diabetes

A

Typically is adolescent presentation
Lean patient
Increase prevalence in those of N.European ancestry

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16
Q

Risk factors for type 1 diabetes

A

Northern European (esp Finnish)
Family history
Genes : HLA-DR3 and HLA-D4
Other autoimmune diseases (i.e Grave’s, coeliac)

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17
Q

Pathogenesis of type 1 diabetes

A

Type IV hypersensitivity reaction as T cells attack the pancreatic beta cells due to their loss of self tolerance
Destruction of the beta cells causes insulin deficiency as it is not secreted by the cells.

Autoantibody formation against islet beta cells

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18
Q

Consequences of the failure of insulin secretion

A

No insulin leads to…
1. No insulin effect on muscle / fat –> impaired glucose clearance and muscle increased muscle/fat breakdown –> less glucose enters the peripheral tissue
2. No hepatic insulin effect –> unrestricted production of glucose and ketones –> more glucose enters the blood
Leads to hyperglycaemia and increase in plasma ketones
Glycosuria and ketonuria

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19
Q

How many beta cells are typically destroyed at the time symptoms develop in type 1 diabetes

A

90%

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20
Q

What would happen if you didn’t treat type 1 diabetes with insulin

A

Increased concentration of glucagon in the circulation (due to the loss of local insulin within the islets there is no negative feedback and inhibition of glucagon release)
State of perceived stress leads to increased cortisol and adrenaline
Progressive catabolic state leads to increased ketones

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21
Q

Clinical presentation of type 1 diabetes (symptoms)

A 
Polyuria and nocturia 
Polydipsia
Unexplained weight loss 
Usually an acute presentation of a young person 
2-6 week history
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22
Q

Why polyuria and nocturia in presentation?

A

Not enough glucose can be reabsorbed by the kidneys as they have reached the renal threshold for maximum resorptive capacity
Increased glucose in the tubule so less water being reabsorbed by osmosis
Increased urine output

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23
Q

Why polydipsia in presentation?

A

Due to loss of electrolytes and fluid in urine

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24
Q

Why is there weight loss in type 1 diabetes presentation

A

Due to fluid depletion and accelerated breakdown of fat and muscle secondary to insulin deficiency
Catabolic state - loss of muscle
Hunger

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25
Q

Signs of type 1 diabetes

A

Glycosuria
Ketonuria
Patient’s breath may smell like pears (ketones)

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26
Q

Complications as the presenting complaint (type 2)

A

Staphylococcal skin infection
Retinopathy
Neuropathy
Erectile dysfunction

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27
Q

What investigations would you do in someone with suspected diabetes

A

Random plasma glucose
Fasting plasma glucose
Oral glucose tolerance test
HbA1c

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28
Q

What is the oral glucose tolerance test

A

Patient fasts for 8-12 hours before you take their blood

Give 75mg of glucose and test blood two hours later

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29
Q

What is HbA1c

A

Measures of the amount of glycerated haemoglobin

It assess the blood glucose level over the past few months (120 days ~ RBC lifespan)

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30
Q

Other tests in your investigation for patients with diabetes that does not include looking at blood glucose levels ?

A

FBC
U&Es
Screen urine for microalbuminuria to assess for kidney disease
blood pH to look for ketoacidosis

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31
Q

What is diagnostic for random plasma glucose

A

11.1mmol/L or more

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32
Q

What is diagnostic for fasting plasma glucose

A

7.0 mmol/L or more

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33
Q

What is diagnostic for HbA1c

A

48 or more

6.5% or more

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34
Q

What do you need to diagnose diabetes

A

Abnormal HbA1c
One abnormal random or fasting plasma glucose + symptoms
Two abnormal results for random and fasting plasma glucose if asymptomatic

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35
Q

Principles of treatment of diabetes (type 1 and 2)

A
  1. control of symptoms
  2. prevention of acute emergencies
  3. identification and prevention of long-term microvascular complications
  4. Patient education on their disease and risks
  5. Maintain a lean weight, don’t smoke and take care of feet
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36
Q

What is the treatment for type 1 diabetes

A

insulin

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37
Q

How is insulin administered

A

subcutaneous injection into the abdomen (fastest absorption rate)

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38
Q

How is insulin activated

A

GI enzymes

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39
Q

What factors can change insulin absorption

A

local tissue reactions
changes in insulin sensitivity
injection site
blood flow

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40
Q

why is it important to change up the injection site for insulin

A

to prevent lipohypertrophy (fatty lumps)

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41
Q

what are the three groups of insulins

A

short-acting insulin
intermediate acting insulin
long acting insulin

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42
Q

What is the first line choice treatment for an insulin regime

A

multiple daily injection basal-bolus insulin
one or more separate daily injections of intermediate acting insulin or long-acting insulin analogue as the basal insulin
alongside multiple bolus injections of short acting insulin before meals

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43
Q

what is the biphasic regime

A

1,2 or 3 insulin injections per day of short acting insulin mixed with intermediate-acting insulin

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44
Q

what is continuous insulin infusion

A

insulin pump
regular or continuous amount of insulin (usually rapid-acting insulin analogue or soluble insulin) delivered by a programmable pump and insulin storage reservoir via a subcutaneous needle

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45
Q

symptoms of hypoglycaemia

A 
hungry 
sweating 
tingling lips 
tremor 
weakness
blurred vision 
easily irritable
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46
Q

complications of insulin therapy

A

hypoglycaemia
insulin resistance - mild
lipohypertrophy
weight gain

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47
Q

define type 2 diabetes

A

caused by decreased insulin resistance with or without decreased insulin secretion

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48
Q

Epidemiology of type 2 diabetes

A

common in all populations enjoying an affluent lifestyle
Increasing incidence due to ageing population and increasing obesity in the west
older patients over 40 yrs old
Increased prevalence in men
More prevalent in south asian, african and caribbean ancestry

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49
Q

Risk factors for type 2 diabetes

A 
family history - first degree relatives. There is a stronger genetic link in type 2 diabetes than type 1 
Increasing age 
obesity 
sedentary lifestyle
ethnicity 
pmh gestational diabetes 
pmh of heart disease or stroke 
high waist circumference
hypertension 
low level of HDL cholesterol 
smoking
excessive alcohol consumption
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50
Q

pathogenesis of type 2 diabetes

A
  1. insulin dependent cells do not respond to insulin (resistance - post receptor)
  2. excess adipose tissue releases FFA that can cause inflammation and influence cell resistance
  3. beta cells undergo hyperplasia and hypertrophy to increase insulin secretion
  4. beta cells secrete amyloid polypeptide and amylin
  5. amylin builds up and aggregates in the islets leading to amyloid deposits in the beta cells
  6. beta cells become dysfunctional and undergo hypoplasia and hypotrophy
  7. impaired insulin secretion
  8. hepatic insulin resistance –> excessive glucose production –> more glucose enters bloodstream
  9. muscle / fat insulin resistance –> decreased glucose uptake after a meal –> impaired glucose clearance and less glucose enters peripheral tissues
  10. hyperglycaemia
  11. glycosuria
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51
Q

what is impaired glucose tolerance

A

HbA1c of 42-47 mmol/L

A unique window for lifestyle intervention

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52
Q

clinical presentation of type 2 diabetes

A 
overweight 
increased visceral fat 
polydipsia 
polyuria 
weight loss 
usually a subacute presentation and onset is over several months or years
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53
Q

why is ketoacidosis rare in type 2

A

low insulin levels are sufficient to suppress catabolism and prevent ketogenesis

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54
Q

investigations of type 2 diabetes

A

same tests as type 1

older patients may present with established complications - retinopathy
patients with severe insulin resistance may have acanthosis nigricans (blackish pigmentation at the nape of the neck and axillae)

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55
Q

Objectives of treatment of type 2

A

manage blood glucose
reduce risk of: CVD mortality and morbidity, CKD, microvascular complications
Weight reduction : increase physical activity and decrease dietary fats

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56
Q

progression of treatment in type 2 diabetes

A 
Lifestyle 
metformin 
dual therapy 
triple therapy 
insulin
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57
Q

lifestyle interventions and advice for type 2 diabetes patients

A

community run lifestyle education programmes e.g DESMOND
Moderately rigorous activity for up to 30 minutes a day
Reduce portion sizes
Diet : low carbohydrate diets, low sugar with high in starch carbohydrates with a low glycaemic index
Stop smoking
Control of blood pressure e.g with ramipril
Hyperlipidaemia control e.g statins
Can give orlistat in obesity (intestinal lipase inhibitor) that reduces absorption of fat from the diet

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58
Q

What is second line therapy for type 2 diabetes

A

metformin

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59
Q

what type of drug is metformin

A

biguanide drug

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60
Q

mechanism of metformin

A

oral drug that works by preventing the production of glucose in the liver, improving the body’s sensitivity towards insulin and reducing the amount of sugar absorbed by the intestines

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61
Q

what does metformin do

A

reduces the rate of gluconeogenesis in the liver
increases cells sensitivity to insulin
weight loss promotion
reduces CVD risk in diabetes

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62
Q

Side effects of metformin

A

anorexia
diarrhoea
nausea
abdominal pain

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63
Q

What drugs can we use as second line dual therapy?

A

sulfonylurea
pioglitazone
incretin based agents (GLP-1 receptor agonist, DPP-4 inhibitors)
SGLT-2 inhibitor

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64
Q

what is the mechanism of sulfonylurea

A

pushes the beta cells in the pancreas to produce more insulin
rapid improvement in glycaemic control

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65
Q

cons to using sulfonylurea

A

overtime it loses its effectiveness (6-8 years)

causes weight gain initially

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66
Q

example of a sulfonylurea

A

gliclazide

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67
Q

what are incretins

A

hormones secreted by intestinal endocrine cells in response to nutrient intake
they influence glucose homeostasis by: glucose-dependent insulin secretion, postprandial glucagon suppression and slowing of gastric emptying

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68
Q

What is the effect of GLP-1 in humans

A

glucose enters gut
GLP-1 hormone is released which increases insulin production and promotes satiety, decreasing appetite
Lowers blood sugars
Broken down by DPP-4

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69
Q

example of a GLP-1 receptor agonist

A

exenatide

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70
Q

mechanism of a GLP-1 receptor agonist

A

increases GLP-1 levels

induces a delay in gastric emptying

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71
Q

benefit of a GLP-1 receptor agonist

A

induces weight loss by 3-4 kg

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72
Q

who can start on GLP-1 receptor agnoists

A

patient has to have a BMI greater than 35

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73
Q

example of a DPP-4 inhibitor

A

sitagliptin

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74
Q

what do DPP-4 inhibitors do

A

small increase in endogenous GLP-1

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75
Q

example of an SGLT-2 inhibitor

A

empagliflozin

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76
Q

mechanism of SGLT-2 inhibitors

A

works on the kidneys by reducing the resorption of glucose in the kidneys at the PCT
increases renal excretion of glucose and decreases blood glucose

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77
Q

when do we use SGLT-2 inhibitors

A

these are increasingly being used as second line treatment for dual therapy after metformin

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78
Q

complications of SGLT-2 inhibitors

A

GU infections due to increased glycosuria
affect women more than men
easily managed and patients need to be reassured about continuing the treatment

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79
Q

side effect of SGLT-2 inhibitors

A

may cause intravascular volume depletion

need to monitor patients for symptoms of hypotension

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80
Q

mechanism of action of pioglitazone

A

increases insulin sensitivity

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81
Q

side effects of pioglitazone

A

hypoglycaemia
fractures
fluid retention
can increase weight

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82
Q

contraindications of using pioglitazone

A

congestive heart failure
osteoporosis
macula oedema

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83
Q

risks of developing diabetic retinopathy

A 
long duration of diabetes 
poor glycaemic control 
hypertensive 
on insulin 
pregnant
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84
Q

what is an effective way of preventing patients developing early diabetic retinopathy

A

eye screening
anyone over the age of 11 with diabetes
photographs are taken and graded

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85
Q

pathogenesis of diabetic retinopathy

A
  1. hyperglycaemia triggers apoptosis of pericytes
  2. causes localised outpouching of capillary walls
  3. microaneurysms form
  4. microaneurysm formation + smooth muscle cell loss can lead to leakages
  5. breach of microaneurysm causes fluid to leak into the retina
  6. fluid is cleared by the retinal veins and leaves behind protein and lipid deposits
  7. retina compensates for loss of cells by growing new glial cells in capillaries
  8. leads to occlusion
  9. pericyte loss causes endothelial cells to increase turnover which can cause thickening (ischaemia)
  10. ischaemia leads to release of vascular growth factors that cause new blood vessels to grow which are prone to haemorrhaging
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86
Q

how can you see evidence of diabetic retinopathy on a photograph

A

red dots = microaneurysms

yellow-white hard exudates blots = protein and lipid deposition in renal veins

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87
Q

treatment for diabetic retinopathy

A

laser treatment aims at stabilising changes
does not improve sight
if given at the correct stage it is very effective

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88
Q

what feature can you see in advanced diabetic retinopathy

A

cotton wool spots are seen in maculopathy

caused by the fibrosis

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89
Q

what are the microvascular complications of diabetes

A

retinopathy
neuropathy
nephropathy

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90
Q

what are the macrovascular complications of diabetes

A

stroke
cardiovascular disease (leading cause of mortality)
peripheral vascular disease

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91
Q

pathogenesis of diabetic nephropathy

A
  1. hyperglycaemia leads to formation of advanced glycosylation endproducts
  2. these accumulate in the basement membrane and cross link with collagen
  3. thickening of basement membrane
  4. membrane becomes more permeable
  5. glomerular hyperperfusion and hyperfiltration occurs
  6. increases likelihood that proteins will pass through
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92
Q

what is the hallmark of the clinical presentation of diabetic nephropathy

A

proteinuria - urine dipstick test

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93
Q

difference between when clinical presentation of diabetic nephropathy in type 1 and type 2 patients

A

type 1 : develops 5-10 years after diagnosis

type 2 : may already be present at the time of diagnosis

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94
Q

ways to slow progression of diabetic nephropathy

A 
about controlling proteinuria by: 
good glycaemic control 
blood pressure control 
blockage of RAAS with ACE-inhibitors 
cholesterol control

need to intervene and treat aggressively to stop declining renal function

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95
Q

example of an ACE-inhibitor

A

Ramipril

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96
Q

Example of a statin

A

simvastatin

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97
Q

why is diabetes a huge risk factor for cardiovascular disease

A

most diabetic patients are dyslipidemic
dyslipidemia is highly correlated with atherosclerosis
atherosclerosis is associated with nearly all CVD

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98
Q

what is peripheral vascular disease

A

decreased perfusion due to macrovascular disease at more distal sites

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99
Q

symptoms of peripheral vascular disease

A

intermittent claudication

rest pain

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100
Q

signs of peripheral vascular disease

A

pulselessness, pain, pallor, paresthesia and paralysis

5 Ps

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101
Q

how to evaluate peripheral vascular disease

A

Doppler pressure studies measures the amount of blood flow through arteries and veins

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102
Q

treatment of PVD

A

stop smoking
walk through the pain
surgical intervention may be needed

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103
Q

what is diabetic neuropathy

A

a decrease in sensation in the glove and stocking distribution
pathogenesis of the pain is unknown

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104
Q

treatment for DN

A

no cure, so most treatment is symptomatic to reduce their pain

  • good glycaemic control
  • paracetamol
  • anticonvulsants e.g gabapentin
  • opioids e.g tramadol
  • IV lignocaine
  • amitriptyline
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105
Q

what is the progression of treatment for diabetic neuropathy

A

work up the analgesics ladder

paracetamol –> gabapentin –> tramadol

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106
Q

Risk factors for developing diabetic neuropathy

A 
hypertension 
smoking 
high HbA1c
duration of diabetes 
high BMI 
increase in triglycerides
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107
Q

consequences of diabetic neuropathy

A

diabetic foot ulceration which can lead to amputation

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108
Q

what is the progression from diabetic neuropathy to amputation

A
  1. neuropathy
  2. trauma
  3. ulcer
  4. failure to heal
  5. infection
  6. amputation
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109
Q

symptoms of diabetic neuropathy

A

pain (burning, paraesthesia, allodynia, worse at night)
autonomic (orthostatic hypotension, constipation, ED)
insensitivity (foot ulceration, infection)

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110
Q

pathophysiology of diabetic foot

A
  1. trauma happens to the foot (patient cannot feel this as have lost sensitivity so have no feeling of pain)
  2. this can lead to ulcer formation
    additionally :
    - because of deformities in the foot there is more pressure on metatarsal heads so calluses build up which can push against healthy skin underneath and damage it
    - can get autonomic nerve damage i.e no sweating so get cracks and fissures and allow infection to sit it
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111
Q

investigation of diabetic foot

A

early recognition is vital!!!!

  1. test sensation
    - 10mg monofilament
    - neurotips
  2. vibration perception
    - tuning fork
  3. ankle reflexes (may be absent)
  4. look at shoes for any foreign bodies
  5. look at the feet - any skin changes e.g pallor, decreased temp
  6. look for the presence of any ulcers
  7. pulses - doralis pedis, posterior tibial
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112
Q

management of diabetic foot

A

educate patient
daily foot inspection
comfortable and therapeutic shoes
regular chiropody to remove callus as haemorrhage and tissue necrosis may occur leading to ulceration

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113
Q

what is the management if the patient has a foot ulcer

A 
MDT clinic every 2 weeks until the ulcer has healed 
pressure relieving footwear 
podiatry 
revascularisation 
antibiotics in infected
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114
Q

treatment if the infected diabetic foot ulcer does not heal

A

amputation

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115
Q

what increases the likelihood of infection in diabetic foot ulcers

A

poorly controlled diabetes impairs the function of polymorphonuclear leukocytes leading to an increased susceptibility of infections

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116
Q

what are the different hormone classes

A

peptide
amine
cholesterol derivatives and steroids

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117
Q

how are peptide hormones transported

A

water soluble, unbound

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118
Q

how to peptide hormones bind

A

cell-surface receptor

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119
Q

action of steroid hormones

A
  1. diffuse through plasma membrane (because they are lipid soluble)
  2. steroid hormone binds to receptors
  3. receptor-hormone complex enters the nucleus
  4. receptor hormone complex binds to glucocorticoid response elements
  5. binding initiates transcription of gene to mRNA
  6. mRNA directs protein synthesis
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120
Q

3 hormone receptor locations

A

cell membrane
cytoplasm
nuclear receptor family

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121
Q

what are the three releasing factors (stimuli) that control hormone secretion

A

humoral stimulus : hormone release caused by altered levels of certain ions or nutrients
neural stimulus : hormone release caused by neural input
hormonal stimulus : hormone release caused by another hormone release (e.g tropic hormone)

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122
Q

location of the pituitary gland

A

bottom of the brain
sits on top of the sella turcica of the sphenoid bone
hypothalamus sits on top of the pituitary

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123
Q

what connects the hypothalamus to the pituitary gland

A

pituitary stalk / infundibulum

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124
Q

what are the 6 hormones secreted by the anterior pituitary gland

A
  1. adrenocorticotropic hormone (ACTH)
  2. Thyroid stimulating hormone
  3. Growth hormone
  4. Luteinizing hormone
  5. Follice stimulating hormone
  6. Prolactin
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125
Q

what are the two hormones stored in the posterior pituitary gland

A
  1. Vasopressin

2. Oxytocin

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126
Q

what are the three distinct layers of the adrenal gland and what hormone do they secrete

A
  1. zona glomerulosa : mineralcorticoids (aldosterone)
  2. zona fasciculata : glucocorticoids (cortisol)
  3. zona reticularis : androgens
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127
Q

what are the classes of BMI

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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128
Q

what is the process of food intake

A
  • take in food
  • energy balance increases
  • fat stores increase
  • insulin and leptin are released
  • these act on the CNS (catabolic effect to increase metabolic activity, increase physical activity and decrease food uptake)
  • if we lose energy the opposite happens
  • leptin and insulin act on the CNS (anabolic which decreases energy expenditure and increase food uptake)
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129
Q

what is satiety

A

feeling of fullness, the disappearance of appetite after a meal

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130
Q

satiety cascade

A
  1. at the time we should be eating we start to have expectations. smell food and see food. increases satiety
  2. start eating because you are hungry and start to become satiated and appetite goes away
  3. food goes down into the mouth and down stomach. stretch receptors and glucose in stomach. there is feedback on the brain to tell brain that you are getting full
  4. stop eating
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131
Q

where is the satiety centre of the brain located

A

ventromedial hypothalamic nucleus

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132
Q

hormone that is secreted in the hypothalamus that increases appetite

A

neuropeptide Y

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133
Q

three main hormones that regulate appetite

A 
leptin (expressed in white fat) 
peptide YY (SI, pancreas, colon)
cholecystokinin (duodenum)
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134
Q

action of leptin

A

binds to leptin receptor and switches off appetite

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135
Q

action of peptide YY

A

inhibits gastric motility and reduces appetite by binding to NPY receptors

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136
Q

action of cholecystokinin

A

binds to receptors in the pyloric sphincter to delay gastric emptying, causes gall bladder contraction and insulin release

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137
Q

what are the two acute metabolic emergencies caused by untreated diabetes mellitus

A

diabetic ketoacidosis

hyperosmolar coma

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138
Q

when does ketogenesis occur

A

In the place of carbohydate shortages when there are high rates of fatty acid oxidation and large amounts of acetyl CoA are generated that exceeds the capacity of the Kreb’s cycle is when ketone formation occurs

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139
Q

pathology of diabetic ketoacidosis

A

occurs in untreated insulin dependent diabetes

  1. reduced supply of glucose to cells caused by a significant decline in circulating insulin (pushes body into starvation like state)
  2. means there is uncontrollable lipolysis and then an increase in production of free fatty acids
  3. increase in fatty acid oxidation
  4. increased production of acetyl-CoA leads to ketone body production that exceeds the ability of peripheral tissue to oxidize them
  5. ketone bodies are a relatively strong acid and their increase in concentration lowers the pH of the blood
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140
Q

main consequence of the acidification of the blood caused by increased concentration of ketone bodies

A

impairs the ability of haemoglobin to bind to oxygen

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141
Q

risk factors for developing ketoacidosis

A 
untreated diabetes 
stopping insulin therapy 
infection 
surgery 
pancreatitis
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142
Q

Clinical presentation of diabetic ketoacidosis

A 
gradual drowsiness
vomiting 
dehydration 
ketotic breath 
Kussmaul's breathing (deep, rapid breathing as a compensatory mechanism)
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143
Q

Tests for diabetic ketoacidosis

A

ECG, Chest X-ray
Urine : dipstick and microscopy culture and sensitivity
Blood : capillary and lab glucose, ketones, pH, U&Es, HCO3-, FBC

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144
Q

diagnosis of diabetic ketoacidosis

A
  1. Acidaemia (venous blood pH < 7.3)
  2. Hyperglycaemia (blood glucose > 11.0mmol/L) or have known DM
  3. Ketonaemia (>3.0mmol/L)
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145
Q

Treatment of diabetic ketoacidosis

A
  1. Immediate ABCs assessment
  2. Replace fluid loss with 0.9% saline IL over 1 hour
  3. Replace deficient insulin
  4. Give insulin with glucose to prevent hypoglycaemia
  5. Restore electrolyte loss and assess the need for potassium
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146
Q

Complications of management of ketoacidosis

A

cerebral oedema
hypokalaemia
coma

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147
Q

why do you get cerebral oedema in diabetic ketoacidosis

A

The osmolar gradient caused by the high blood glucose results in water shift from the intracelluar fluid (ICF) to the extracellular fluid (ECF) space

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148
Q

prevention of diabetic ketoacidosis

A

talk to the patient and evaluate compliance and educate about triggers

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149
Q

what is hyperosmolar hyperglycaemic state

A

hyperglycaemia causes an osmotic diuresis (increased urine) with hyperosmolarity leading to an osmotic shift of water into the intravascular compartment resulting in severe intracellular dehydration

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150
Q

is the ketogenesis in hyperosmolar hyperglycaemic state

A

No
insulin levels are reduced but still sufficient to inhibit hepatic ketogenesis
So no acidosis is either pH > 7.3

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151
Q

who is most likely to develop hyperosmolar hyperglycaemic state

A

older type 2 diabetic patients

152
Q

risk factors for developing hyperosmolar hyperglycaemic state

A

infection - particularly pneumonia

inadequate insulin or oral antidiabetic therapy

153
Q

symptoms of hyperosmolar hyperglycaemic state

A

early symptoms of generalised weakness, leg cramps or visual impairment
focal neurological symptoms e.g weakness
dehydration (dry mouth, decreased skin turgor or sunken eyes)

154
Q

signs of hyperosmolar hyperglycaemic state

A

severe dehydration (dry mouth, decreased skin turgor or sunken eyes)
THREE CHARACTERISTIC FEATURES
1. Hypovolaemia
2. Hyperglycaemia (glucose > 30.0 mmol/L)
3. Hyperosmolality (effective serum osmolality > 320mmol/kg)

155
Q

Diagnosis of hyperosmolar hyperglycaemic state

A
  1. Hypovolaemia
  2. Hyperglycaemia (glucose > 30.0 mmol/L)
  3. Hyperosmolality (effective serum osmolality > 320mmol/kg)

urine dipstick shows heavy glycosuria
total body K+ is low as a result of osmotic diuresis

156
Q

treatment goals of hyperosmolar hyperglycaemic state

A

normalise osmolality
replace fluid and electrolyte loss
normalise blood glucose

157
Q

the treatment for hyperosmolar hyperglycaemic state

A

give low dose IV insulin

fluid replacement with 0.9% saline to restore circulating volume and reverse dehydration

158
Q

what happens to dietary iodide

A

oxidised to iodine in the thyroid gland by the enzyme thyroid peroxidase
iodine is then used to produced T4 and T3

159
Q

which is the more potent thyroid hormone produced

A

T3

T4 is considered to be a prohormone

160
Q

how does T3 and T4 travel in the plasma

A

it is protein bound to thyroxine-binding globulin

161
Q

what does the free T3 and T4 do

A

free T3 and T4 are considered to be active and increase cell metabolism via nuclear receptors

162
Q

what is the thyroid pituitary axis

A
  • hypothalamus secretes Thyrotropin-releasing hormone
  • TRH stimulates the production of thyroid stimulating hormone from the anterior pituitary gland
  • TSH increases production and release of T4 and T3 from the thyroid which both exert a negative feedback effect on TSH and TRH production
163
Q

What are the three types of clinical thyroid disease

A

Secretory malfunction : hyper and hypothyroidism
Swelling of the entire gland : goitre
Solitary mass : 1 large nodule in a nodular goitre, adenoma or carcinoma

164
Q

what is hyperthyroidism

A

disease of which there are excess thyroid hormones circulating in the blood

165
Q

Symptoms of hyperthyroidism

A 
diarrhoea 
weight loss 
increased appetite 
sweats 
heat intolerance 
palpitations 
tremor 
irritability 
oligomenorrhea 
anxiety
166
Q

what is oligomenorrhea

A

infrequent periods

167
Q

cause of diarrhoea as a symptom of hyperthyroidism

A

increased effectiveness of the bowel

168
Q

cause of weight loss as a symptom of hyperthyroidism

A

muscle breakdown

169
Q

actual names of T3 and T4

A

thyroxine (T4) and triiodothyronine (T3)

170
Q

what do the thyroid hormones do (basic)

A

influence the metabolism of your body cells

171
Q

Clinical signs of hyperthyroidism

A 
Fast/irregular pulse 
Warm, moist skin
Fine tremor
Palmar erythema (redness to both palms) 
thin hair 
lid lag : eyelid lags behind the eye's descent as patient watches your finger descend slowly 
lid retraction : stare
172
Q

specific clinical signs of Grave’s disease

A

Exophthalmos : bulging of the eye anteriorly out of the orbit
pretibial myxoedema : localised lesions of the skin resulting from the deposition of hyaluronic acid
thyroid acropachy (rare) : clubbing, painful finger and toe swelling.

173
Q

what causes exophthalmos in Grave’s disease

A

infiltration of lymphocytes into orbital tissue stimulates the release of cytokines
Cytokines promote the release of mucopolysaccharides from fibroblasts
Resulting hyperosmotic shift leads to oedema of the orbital fat and extraocular muscles
Eyeball is forced anteriorly

174
Q

how many people with Grave’s exhibit exophthalmos

175
Q

Investigations of hyperthyroidism

A 
thyroid function test to confirm biochemical hyperthyroidism 
Clinical history (physical signs are usually sufficient for diagnosis) 
Supporting tests
176
Q

Tests for hyperthyroidism and results

A

primary hyperthyroidism : increased free T3 and T4 and suppressed TSH
secondary hyperthyroidism (e.g adenoma) : increased free T4 and T3 but there is an inappropriate high TSH
Thyroid antibodies : TPO, Tg and TRAb
Isotope uptake scan

177
Q

what are the thyroid antibodies

A

TPO : antithyroid peroxidase antibody
Tg : antithyroglobulin antibody
TRAb : TSH receptor antibodies

178
Q

Commonest cause of hyperthyroidism

A

Grave’s disease

179
Q

Pathogenesis of Grave’s disease

A

production of an autoantibody of the IgG class which binds and activates G-protein coupled receptors which cause smooth thyroid enlargement and increased hormone production (especially T3) and react with orbital autoantigens.

180
Q

In Grave’s disease can the autoantibodies cross the placenta

181
Q

Risk factors for developing Grave’s disease

A

Genetic : HLA-DR3 and female
Environmental : smoking, diet, infection
Postpartum
Associated with other autoimmune conditions : T1DM, addison’s, vitiligo

182
Q

Causes for Hyperthyroidism

A

Grave’s disease
Toxic multinodular goitre
Toxic, functioning adenoma
Exogenous : iodine excess (food contamination, contrast media (can cause thyroid storm if patient is already hyperthyroid))

183
Q

How does toxic multinodular goitre cause hyperthyroidism

A

1 or 2 nodules in a goitre may develop hypersecretory activity
Elderly and iodine deficient areas (derbyshire neck)

184
Q

How does a toxic functioning adenoma cause hyperthyroidism

A

solitary nodule produces T3 and T4

less than 1% of adenomas

185
Q

Three ways can treat hyperthyroidism and the order you would try

A
  1. Drugs
  2. Radioiodine
  3. Surgery
186
Q

What is the drug regime in hyperthyroidism

A
  1. Beta-blockers to rapidly control symptoms
  2. Antithyroid medication - CARBIMAZOLE
    - titration regime for 12-18 months
    - block and replace - give carbimazole to suppress thyroid function + thyroxine replacement to restore to euthyroid state
187
Q

how does carbimazole work

A

inhibits conversion of T4 to T3

188
Q

how many patients will relapse on the drug treatment for hyperthyroidism

A

approx 50%

usually younger men than smoke

189
Q

what is the next step if there is a sub-optimal response to the drug treatment in hyperthyroidism

A

Radioiodine

Surgery (if there is a sub-optimal response to radioiodine or patient is pregnant)

190
Q

How does radioiodine work in hyperthyroidism

A

radioactive iodine is given to the patient as a drink and is actively transported into thyroid follicular cells
Causes necrosis of follicular cells

191
Q

What surgery for hyperthyroidism

A

partial or sub total thyroidectomy

192
Q

side effects of of carbimazole

A

rash, hepatitis, thrombocytopenia, vasculitis

can cause bone marrow suppression and agranulocytosis in 0.5% of patients

193
Q

Complications of hyperthyroidism

A

heart failure
angina
AF
osteoporosis

194
Q

symptoms of hypothyroidism

A 
tired 
lethargic 
cold intolerance 
increased weight 
constipation 
Menorrhagia 
Hoarse voice 
Decreased memory and cognition 
Muscle cramps 
Weakness 
Dry skin
195
Q

Clinical signs of hypothyroidism

A 
BRADYCARDIC 
Bradycardic
Reflexes relax slowly 
Ataxia
Dry thin hair
Yawning 
Cold hands
Ascites 
Round puffy face - myxodermic face 
Defeated demeanor 
Immobile (muscle weakness)
196
Q

Diagnosis for hypothyroidism

A

Thyroid function test
Primary hypothyroidism : low T4 and T3. TSH is high.
Secondary hypothyroidism : reduced T4 and T3. TSH may be inappropriately low
Increased cholesterol and triglyceride

197
Q

Causes of primary hypothyroidism

A 
Hashimoto's thyroiditis 
Atrophic thyroiditis 
Iodine deficiency
Post radio iodine treatment 
Drug induced (amiodarone, lithium)
198
Q

what antibodies can be detected in Hashimoto’s thyroiditis

A

antithyroid peroxidase

antithyroglobulin

199
Q

Treatment of hypothyroidism

A

synthetic L-thyroxine (T4)

200
Q

why are the symptoms of thyroid disease so various and subtle

A

almost all cell nuclei have receptors showing a high affinity for T3

201
Q

which tumours of the thyroid are treatable and usually curable?

A

differentiated tumours

papillary / follicular

202
Q

which tumours of the thyroid are less common, more aggressive and have a much poorer prognosis?

A

poorly differentiated

medullary / anaplastic

203
Q

how to diagnose a thyroid tumour?

A

ultrasound is the first line diagnostic procedure
fine needle aspiration cytology
thyroid functioning test

204
Q

most common cancer of the thyroid gland

A

papillary adenocarcinoma

205
Q

risk factors for thyroid cancers

A 
exposure to ionising radiation 
family history 
female 
asian 
obesity
206
Q

presentation of thyroid cancer

A

thyroid nodule

hard and fixed nodules are more suggestive of malignancy

207
Q

red flags in thyroid nodule presentation that could be cancer

A

family history
history of previous irradiation
child patient
unexplained hoarseness associated with goitre
painless thyroid mass enlarging rapidly over a period of weeks
palpable cervical lymphadenopathy

208
Q

causes of pituitary disease

A 
benign pituitary adenoma 
craniopharyngioma
trauma 
apoplexy
sheehans
209
Q

what effects do pituitary tumours have

A
  • cause pressure on local structures
  • put pressure on the pituitary gland
  • may be a functioning pituitary tumour
210
Q

complication of a pituitary tumour causing pressure on local structures

A

can cause bitemporal hemianopia due to compression at the optic chiasm
patients have early desaturation to red when there is increased pressure on the optic chiasm (test using red needle)

211
Q

what happens if there is a tumour that is putting pressure on the pituitary gland

A

lack of function of the pituitary gland

hypopituitary man

212
Q

signs of hypopituitary man

A

pale (loss of testosterone)
no body hair (loss of testosterone)
centrally obese (loss of function of growth hormone)

213
Q

Examples of conditions caused by a functioning pituitary tumour

A

Cushing’s
Acromegaly
Prolactinoma

214
Q

what is Cushing’s disease (definition)

A

chronic, excessive and inappropriate elevated levels of circulating plasma glucocorticoids (cortisol)

215
Q

what is the difference between cushing’s disease and cushing’s syndrome

A

cushing’s disease : make too much of ACTH hormone which causes adrenal glands to make more cortisol
cushing’s syndrome : adrenal glands have a tumour making too much cortisol

216
Q

why is cushing’s disease important to spot in children

A

it is virtually the only disease that can make a child put on weight but not grow

217
Q

causes of Cushing’s

A

Tumour of the pituitary gland making too much ACTH
Ectopic tumour causing increased ACTH secretion
Adrenal tumour making too much cortisol (syndrome)
Exogenous steroids

218
Q

Pathophysiology of Cushing’s disease

A

Tumour in anterior pituitary gland causes an increase of ACTH to be released
Increased ACTH in the body which acts on the adrenal gland to cause an increase in cortisol
Cortisol acts on the hypothalamus and pituitary gland to suppress ACTH and decreased production of corticotropin releasing hormone

219
Q

Pathophysiology in Cushing’s syndrome

A

Tumour in the adrenal gland causing increased cortisol production
Low ACTH and CRH

220
Q

Symptoms of Cushing’s

A 
Fat 
- increased fat
- central obesity
- moon face 
- weight gain 
- buffalo hump
Protein 
- catabolism
- muscle weakness and wasting 
- thin skin (striae on abdomen) + easy bruising 
Androgenic 
- Hirsutism 
- Acne
221
Q

what can also happen if there is increased cortisol in the body

A

immunosuppression

222
Q

Clinical features of Cushing’s

A
  1. carbohydrate metabolism - impaired glucose tolerance
  2. electrolyte disturbance - sodium retention, hypertension
  3. immune suppression
  4. central effects - malaise, depression
  5. suppressed gonadal function - oligo/amenorrhoea, impotence, loss of libido
223
Q

4 important features of Cushing’s

A

Think skin
Easy bruising
Decreased linear growth in children
Weakness

224
Q

2 steps to diagnosing Cushing’s

A
  1. need to confirm if the patient has increased cortisol

2. investigation into the cause of excess cortisol

225
Q

What are the main screening tests to detect if a patient has increased serum cortisol

A
  1. Urinary free cortisol test
  2. Low dose dexamethasone suppression tests
  3. Late night/midnight salivary cortisol
  4. Late night/midnight plasma serum cortisol
226
Q

Why would you have an increased urinary cortisol in Cushing’s

A

Cortisol is bound to cortisol binding globulin and albumin. If these carriers are saturated then the cortisol can spill out into the kidneys so need to measure the amount of cortisol in the urine

227
Q

What is a low dose dexamethasone suppression test

A

Giving a synthetic steroid that is trying to suppress the tumour
Taken at 11pm then cortisol measurement at 8am next day
Serum cortisol > 50nM (normal)

228
Q

Why do you take a late night/midnight salivary cortisol

A

In Cushing’s you lose the normal circadian rhythm
Normally cortisol levels are very low in the night
In Cushing’s the levels are elevated

229
Q

Results that suggest Cushing’s disease in a late night/midnight serum cortisol

A

Sleeping > 50nM

230
Q

If you get an abnormal result for cortisol and it is raised what is the next investigation

A

Measure plasma ACTH

This determines if it is ACTH independent or ACTH dependent Cushing’s syndrome

231
Q

You find that it is ACTH independent Cushing’s syndrome, what are the next investigations for diagnosis ?

A

Adrenal imaging with CT

  • Adrenal lesion –> adenoma or carcinoma
  • No adrenal lesion –> Exogenous steroids, PPNAD
232
Q

You find that it is ACTH dependent Cushing’s syndrome what are the next investigations for diagnosis?

A

Pituitary MRI and CRH test (injection of CRH)

  1. Adenoma + positive CRH response + suppression on high dose dexamethasone suppression test –> CUSHING’S DISEASE
  2. Small/no adenoma + No ACTH gradient –> CT/MRI thorax + abdomen –> Ectopic ACTH
233
Q

what is the difference between low dose dexamethasone and high dose dexamethasone suppression tests

A

An abnormal response to the low-dose test may mean that you have abnormal release of cortisol (Cushing syndrome). The high-dose test can help tell a pituitary cause (Cushing disease) from other causes.

234
Q

Results of the dexamethasone suppression tests in Cushing’s disease.

A

Low-dose test – no decrease in blood cortisol

High-dose test – expected decrease in blood cortisol

235
Q

Management of Cushing’s disease

A

Transsphenoidal surgery + radiotherapy (adjuvant therapy)

236
Q

Management of ectopic tumour, adrenal adenoma/carcioma causing Cushing’s?

A

Adrenalectomy

237
Q

Potetial complication from an adrenalectomy?

A

Nelson’s syndrome

- enlargement of an ACTH producing tumour in pituitary gland following surgical removal of the adrenal glands

238
Q

Pathogenesis of acromegaly

A

Increased secretion of growth hormone from a pituitary tumour
Growth hormone stimulates bone and soft tissue growth through increased secretion of insulin-like growth factor-1 from the liver
It is characterised by ongoing, inappropriate high levels of growth hormone

239
Q

When does gigantism occur?

A

If agromegaly occurs before the fusion of the epiphysis

240
Q

symptoms of acromegaly

A
  • acroparesthesia (tingling, prickling, burning, or numb feeling in the hands or feet.)
  • changes in facial features (thickening of the jaw and nasal bridge)
  • larger hands/feet (increase in ring size/shoe size)
  • amenorrhoea
  • headache (change in circulation of IGF-1 in CSF)
  • excessive sweating
  • Backache
  • snoring
241
Q

Signs of acromegaly

A
  • increased hand, foot and jaw growth
  • wide nose
  • macroglossia (unusually large tongue)
  • puffy lids, eyelids and skin
  • skin darkening
  • obstructive sleep apnoea
242
Q

Complications and comorbidities associated with acromegaly

A

impaired glucose tolerance
vascular changes - increased risk of IHD and stroke
Arthritis

243
Q

Investigations to diagnose acromegaly

A
  1. Randome Growth Hormone and IGF-1
    - if less than 0.4ng/ml = excluded
    - if abnormal go to step 2
  2. 75mg glucose tolerance test
    - if the lowest GH value during OGTT is above 1ug/L then agromegaly is confirmed
244
Q

Why do we do a OGTT in acromegaly testing

A

normally GH secretion is inhibited by high glucose and GH is hardly detectable. In agromegaly GH fails to be suppressed

245
Q

What is the three line strategy for the treatment of acromegaly?

A

surgery
somatostatin analogues
pegvisomant

246
Q

what is surgical management of acromegaly (first line treatment)

A

transsphenoidal excision of the pituitary tumour
success of surgery is dependent on the size of the tumour (microadenomas have a higher cure rate) and the skill of the surgeon

247
Q

complication of pituitary surgery in acromegaly

A

hypopituitarism

248
Q

what is the second line treatment for acromegaly

A

somatostain agonists control GH and IGF-1

249
Q

examples of somatostatin analogues

A

octreotide or lanreotide

250
Q

what is the third line treatment for acromegaly

A

pegvisomant

251
Q

mechanism of action of pegvisomant

A

growth hormone competitive antagonist that binds to growth hormone receptors and inhibits dimerization of GH
act at the liver
used if resistant or intolerant to SSA

252
Q

production of prolactin

A

prolactin is produced in the lactotroph cells of the anterior pituitary gland. production is stimulated by : dopamine receptor antagonists, suckling infant,

253
Q

what inhibits prolactin production

A

dopamine!
dopamine binds to type 2 dopamine receptors that are functionally linked to membrane channels and G proteins which suppress the high intrinsic secretory activity and lactrotroph proliferation.
this is tonic inhibition

254
Q

cause of prolactinoma

A

lactotroph cell benign tumour of the pituitary

255
Q

clinical features of prolactinoma

A 
galactorrhoea - excessive / inappropriate secretion of breast milk
menstrual irregularity
infertility 
low libido 
erectile dysfunction
local effects of tumour
256
Q

when should you not measure a patient’s prolactin

A

when the patient is on antidopaminergic drugs

need to do a careful drug history

257
Q

Management of prolactinoma

A 
Dopamine agonists (cabergoline, bromocriptine) 
shrinks the tumours
258
Q

Possible complications of prolactinoma

A

osteoporosis

reduced fertility

259
Q

what is conn’s syndrome

A

rare health problem that occurs when the adrenal glands make too much aldosterone

260
Q

what is conn’s syndrome also known as

A

primary hyperaldosteronism

261
Q

pathophysiolgy of conn’s syndrome

A

excess production of aldosterone, independent of the RAAS system causing increased sodium and water retention and decreased renin release

262
Q

symptoms of conn’s syndrome

A

asymptomatic or signs of hypokalaemia, weakness, cramps, paraesthesiae, polyuria, polydipsia

263
Q

causes of conn’s syndrome

A

solitary aldosterone producing adenoma

conn’s is the cause for 60% of primary hyperaldosteronisms

264
Q

Tests for conn’s syndrome

A

U&E
Renin
Aldosterone
CT/MRI maybe to find the site of the adenoma
If patient has an adrenal mass - will have adrenal vein sampling

265
Q

Treatment for conn’s syndrome

A

laprascopic adrenalectomy

266
Q

briefly describe the hypothalamo-pituitary adrenal axis

A
  1. hypothalamus releases corticotropin releasing hormone which acts on the anterior pituitary gland
  2. anterior pituitary gland releases ACTH that enters the circulation
  3. ACTH travels to the adrenal cortex and stimulates it to secrete: aldosterone, cortisol and androgens
  4. increase in cortisol in the circulation has a negative feedback on the hypothalamus
267
Q

what is the function of aldosterone

A

increases sodium and water retention resulting in increase in blood pressure

268
Q

what is addison’s disease

A

primary adrenal cortex insufficiency

269
Q

biggest causes of addison’s disease

A

autoantibodies being produced against adrenal cortex cells +/- autoantibodies against the 21-hydroxylase enzyme.
Autoimmune attack causes damage and leads to cortisol and aldosterone deficiency

decrease in minceralcorticoids leads to hypotension and tachycardia

270
Q

other causes of addison’s disease

A 
infection - TB is most common worldwide 
adrenal cortex malignancy 
secondary malignancy of the adrenal cortex from mets 
lymphoma 
infiltration diseases : amyloidosis 
Iatrogenic causes
271
Q

symptoms of addison’s disease

A 
tiredness,
dizziness,
weight loss
abdominal pain
decreased libido (women only)
nausea + vomiting 
lean 
arthralgia and myalgia
272
Q

signs of addison’s disease

A 
low grade fever
dehydration 
postural hypotension 
tachycardia 
pigmentation and pallor - buccal mucosa 
generalised hyperpigmentation

Need a high level of suspicion for diagnosis!! Think of addison’s in all with unexplained abdominal pain or vomiting

273
Q

Investigations results of addison’s disease (biochemistry)

A

Biochemistry

  • decreased Na+
  • Increased K+
  • decreased glucose due to decreased cortisol
  • eosinophilia
  • increased Ca2+
274
Q

Tests to do when investigating someone with addison’s disease

A
  • Synacthen test
  • 9am ACTH
  • 21-hydroxylase adrenal autoantibodies
  • plasma renin and aldosterone to assess mineralcorticoid status
275
Q

what is the synacthen test (addison’s)

A

do plasma cortisol before and 1/2 hour after tetracosacride

Addison’s is excluded if 30min cortisol is > 550nmol/L

276
Q

Results of a 9am ACTH test to suggest addison’s disease

A

cortisol is low

ACTH is innappropriately high

277
Q

Treatment for Addison’s disease

A

Hydrocortisone 2 or 3 times daily

replace aldosterone with fludrocortisone

278
Q

what are the sick day rules

A

what actions patients who are on steroids need to take during illness and stressful situations

  • if unwell - double the dose
  • if vomiting or increasingly unwell take emergency injection of hydrocortisone IM
279
Q

what is secondary adrenal insufficiency

A

inadequate pituitary or hypothalamic stimulation of the adrenal glands
No autoantibodies

280
Q

what are the two types of secondary adrenal insufficiency

A
  1. diseases that cause a total absence of ACTH –> destruction of hypothalamus/pituitary gland (e.g pituitary tumours, surgery to remove a pituitary tumour, radiation therapy to the pituitary)
  2. diseases that cause a suppression of ACTH
281
Q

what is the most common cause of secondary adrenal insufficiency

A

iatrogenic due to long term steroid therapy leading to suppression of the pituitary adrenal axis. Only becomes apparent on the withdrawal of steroids

282
Q

symptoms of secondary adrenal insufficiency

A 
severe fatigue 
loss of appetite 
weight loss 
nausea &amp; vomiting 
muscle weakness
283
Q

differences between Addison’s disease and secondary adrenal insufficiency

A

aldosterone is usually present, so low blood pressure and muscle spasms are not as likely
no hyperpigmentation

284
Q

diagnosis and tests in secondary adrenal insufficiency

A

blood tests - normal K+, blood sugar may be low but not always, FBC is usually normal
tests are usually same as addison’s but there are some differences
- ACTH are low or normal
- Plasma renin and aldosterone levels are usually unaffected
-insulin tolerance test is occasionally used to confirm a diagnosis

285
Q

treatment for secondary adrenal insufficiency

A

hydrocortisone

286
Q

what is the common presentation of adrenal crisis

A 
hypotension and cardiovascular collapse 
fatigue 
fever 
hypoglycaemia 
hyponatraemia and hyperkalaemia
287
Q

treatment for adrenal crisis

A

Bloods if possible for ACTH and cortisol
Hydrocortisone immediately IV or IM
fluids

288
Q

define hyperkalaemia

A

plasma potassium in excess of 5.5mmol/L

289
Q

what is regarded as severe hyperkalaemia

A

plasma potassium > 6.5 mmol/L

290
Q

Causes of hyperkalaemia

A

Renal - AKI, CKD, ACE inhibitors
Increased circulation of potassium - exogenous or endogenous (massive tissue damage, fresh water drowning)
Shift from the intracellular to extracellular space (acidosis e.g DKA)

291
Q

reasons why a lab result for potassium showing hyperkalaemia may not be valid?

A

tourniquet has been on for a prolonged amount of time
difficulting collecting sample
length of storage
test tube haemolysis

292
Q

symptoms of hyperkalaemia

A

weakness, fatigue, may present with muscular paralysis or SOB or palpitations

293
Q

signs of hyperkalaemia

A

occasional bradycardia due to heart block
tachypnoea from resp muscle weakness
muscle weakness and flaccid paralysis

294
Q

concerning signs and symptoms in hyperkalaemia

A 
fast irregular pulse 
chest pain 
weakness
palpitations 
light headedness
295
Q

investigations for hyperkalaemia

A

blood tests

  • urea
  • other electrolytes
  • creatinine
  • ABG - looking for metabolic acidosis
296
Q

ECG changes in hyperkalaemia

A
  • tall tented t wave
  • longer PR interval
  • reduced or no p waves
  • widening of QRS complex

usually only seen in severe cases

297
Q

Management of hyperkalaemia

A

EMERGENCY

  • ABCDE
  • ABG
  • ECG
  • full history including drug history
  • Reduce the potassium
298
Q

Treatment of hyperkalaemia

A
  • give calcium gluconate to protect the cardiac membrane if there are ECG changes
  • Insulin-dextrose infusion
299
Q

define hypokalaemia

A

serum concentration of potassium < 3.5 mmol/L

300
Q

3 causes of hypokalaemia

A
  • severe vomiting
  • diarrhoea
  • Cushing’s syndrome/steroids
  • diuretic therapy
  • pyloric stenosis
  • Conn’s syndrome
301
Q

what is hypokalaemia often accompanied by

A

metabolic alkalosis due to hydrogen ion shift into the intracellular compartment

302
Q

presentation of hypokalaemia

A 
mild cases tend to be asymptomatic 
in more severe cases: 
- lassitude (lack of energy) 
- generalised weakness and muscle pain 
- constipation 
- cardiac dysrhythmias
303
Q

investigations of hypokalaemia

A

Blood test

ECG

304
Q

what ECG changes can be picked up in hypokalaemia

A

small/inverted T waves
long PR interval
depressed ST segments

305
Q

Treatment of mild hypokalaemia

A

oral K+ supplement

306
Q

treatment of severe hypokalaemia

A

IV potassium
give cautiously!

severe is defined as serum potassium < 2.5 mmol/L

307
Q

what is the equation for plasma osmolality

A

plasma osmolality = (2x [Na+]) + glucose + urea

308
Q

define hyponatraemia

A

low sodium concentration in the blood
depends on both the amount of Na+ and water present in the circulation
serum sodium < 135mmol/L

309
Q

what do the symptoms of hyponatraemia depend on

A

the onset of symptoms

the quicker the onset the greater the symptoms

310
Q

tests when hyponatraemia presents

A

plasma osmolality
urine osmolality
plasma glucose
urine sodium

311
Q

why are there different approaches in acute vs chronic hyponatraeima

A

acute - rapid correction

chronic - CNS adapts so the correction must be slow

312
Q

what is syndrome of inappropriate secretion of ADH

A

excessive secretion of ADH from the posterior pituitary gland or another source
by increasing water retention, ADH causes dilution of the blood and decreases the concentration of solutes

313
Q

what is the normal physiology of ADH

A
  1. ADH produced by hypothalamus in response to increased serum osmolality detected by the osmoreceptors
  2. ADH is transported to the posterior pituitary gland
  3. ADH is released into the circulation
  4. ADH travels to kidneys and binds to ADH receptors on the CD
  5. binding of ADH causes aquaporin-2 channels to move from the cytoplasm into the apical membrane of the tubules
  6. water reabsorption out of the collecting ducts back into the blood stream
  7. results in a decrease in volume and increase in osmolality of the urine produced
  8. reduction in serum osmolality
  9. reduction in serum osmolality detected by the hypothalamus and results in decreased production of ADH (negative feedback)
314
Q

pathogenesis of syndrome of inappropriate secretion of ADH

A

lack of the negative feedback mechanism
inability to reduce or stop ADH production
leads to abnormally low levels of serum sodium (due to the excess water resorption) and relatively high levels of urine sodium

315
Q

causes of syndrome of inappropriate secretion of ADH

A 
Malignancy 
- small cell lung cancer 
CNS disorders 
- meningitis 
- subarachnoid haemorrhage 
Chest disease 
- TB
- atypical pneumonia 
Endocrine disease 
- hypothyroidism 
Drugs 
- carbamazepine
- opiates 
-SSRIs
316
Q

3 symptoms of SIADH (mild)

A 
nausea 
vomiting 
headache
anorexia 
lethargy
317
Q

3 symptoms of SIADH (moderate)

A

muscle cramps
weakness
confusion

318
Q

3 symptoms of SIADH (severe)

A

drowsiness
seizures
coma

319
Q

why do some chronically hyponatremic patients have very low serum sodium concentrations but are completely asymptomatic ?

A

Cerebral adaptation

  1. ECF hypoosmolality
  2. water moves into the brain in response to osmotic gradients producing brain oedema
  3. in response to swelling the brain expels electrolytes and organic osmolytes
  4. water loss accompanies the loss of these solutes, reduing swelling
  5. if hypo-osmolality is sustained, brain volume normalises and the brain becomes adapted to hyponatraemia
320
Q

3 signs of SIADH

A 
decreased levels of consciousness 
cognitive impairment 
brain stem herniation (severe, can result in coma/resp arrest) 
focal or generalised seizures 
hypervolaemia 
- pulmonary oedema 
- peripheral oedema
- raised jugular venous pressure
321
Q

investigations in SIADH

A
  • fluid status (in SIADH, patient is either euvolemic or hypervolaemic)
  • serum sodium
  • serum potassium
  • urine osmolality (will be high it is the excess ADH causing water retention!! it is usually low if serum osmolality is low)
322
Q

what does there need to be to diagnose SIADH

A
  • no dehydration
  • not oedematous
  • concentrated urine
  • hyponatraemia
  • low plasma osmolality
323
Q

management of SIADH

A
  • treat the underlying cause
  • fluid restriction used to increase serum sodium concentrations
  • demeclocycline
  • replace sodium (IV or orally)
  • vasopressin receptor antagonist (but v expensive)
324
Q

complication of replacing sodium concentration too quickly in patients with hyponatraemia

A

central pontine myelinolysis (permanent damage to the myelin sheath in the brain stem)

325
Q

definition of hypernatremia

A

serum sodium concentration of > 145mmol/L

326
Q

causes of hypernatremia

A

dehydration (inadequate water intake, DI, thirst impairment)
hypotonic fluid loss (dermal losses e.g burns, GI losses e.g D&;V, urinary losses e.g diuretics)
hypertonic sodium gain (iatrogenic e.g tube feeding, excess salt ingestion)

327
Q

5 Signs and symptoms of hypernatremia

A 
Lethargy
Thirst 
Polydipsia
Polyuria
Weakness
Irritability 
Confusion 
Fits 
Coma 
Signs of dehydration
328
Q

Investigations for hypernatremia

A

Check serum sodium, potassium, urea, creatinine etc.

329
Q

Lab results for hypernatremia

A
  • increased Na+
  • increased packed cell volume
  • increased albumin concentration
  • increased urea
330
Q

Management for hypernatremia

A

Treat any underlying disorder if possible

Give water to slowly replace dehydration (orally if possible)

331
Q

what is diabetes insipidus

A

the passage of large volumes of dilute urine (more than 3L a day) due to impaired water reabsorption by the kidney, because of reduced ADH secretion from the posterior pituitary (cranial DI) or impaired response of the kidney to ADH (nephrogenic DI)

332
Q

what is cranial diabetes insipidus

A

occurs due to decreased circulating levels of vasopressin

333
Q

what is nephrogenic diabetes insipidus

A

anything that interferes with the binding of vasopressin to their receptors or damages the kidney leading to an impaired response by the kidney to ADH

334
Q

3 acquired causes of cranial diabetes insipidus

A 
idiopathic 
tumours : craniopharyngioma, germinoma 
Trauma to hypothalamus or posterior pituitary 
Neurosurgery 
Infections : meningitis 
Vascular - Sheenan's sickle cell
335
Q

name a genetic cause of cranial diabetes insipidus

A

Wolfram syndrome

336
Q

name a familial cause of nephrogenic diabetes insipidus

A

X linked, V2 receptor defect

Autosomal recessive : aquaporin 2 defect

337
Q

name 3 acquired causes of nephrogenic diabetes insipidus

A

osmotic diuresis
Drugs (lithium, tetracycline)
Chronic renal failure
post-obstructive uropathy

338
Q

Symptoms of diabetes insipidus

A

excessive urination, polyuria > 3L/day
excessive thirst esp for ice water, polydipsia
nocturia
dehydration -headache/dizziness/dry mouth

339
Q

signs of diabetes insipidus

A

hypotension
dilute urine
reduced capillary fill time
dehydration

340
Q

Investigations and tests in diabetes insipidus

A
  • FLUID DEPRIVATION TEST
  • measure urine output
  • glucose test to exclude DM - dipstick urine
  • U&Es
  • serum and urine osmolalities
341
Q

when should you do the fluid deprivation test

A

for diagnosis of diabetes insipidus

only do when urine output has been confirmed as over 3L a day !

342
Q

what does the fluid deprivation test test for

A

tests the ability of the kidneys to concentrate urine for diagnosis of DI and then to localise the cause

343
Q

outline the two steps of the fluid deprivation test

A

STAGE 1

  • Empty bladder, no drinks, only dry food
  • weigh hourly
  • if more than 3% of weight loss during test, order serum osmolality if more than 300mOsm/kg –> stage 2

STAGE 2
- give desmopressin IM

344
Q

how can the fluid deprivation test determine cranial from nephrogenic DI

A

If after stage 2…
1. urine osmolality increases –> CRANIAL DI because the cause is a lack of vasopressin, so giving the synthetic form normalises the urine osmolality

  1. urine osmolality stays same –> NEPHROGENIC DI
    kidneys are not able to respond to vasopressin so is unable to respond to the synthetic form
345
Q

Management of cranial DI

A

MRI of head
Test anterior pituitary function
Give desmopressin

346
Q

management of nephrogenic DI

A

treat the cause / stop any causative drugs (e.g lithium)
advise patient to maintain adequate fluid intake
correct any metabolic derangements
Bendroflumethiazide can reduce the action of prostaglandins which can inhibit the action of vasopression on the kidneys

347
Q

what is the equation for corrected calcium

A

corrected calcium = total serum calcium + 0.02 x (40- serum albumin)

348
Q

why do we have to correct calcium when investigating hypocalcaemia

A

need to establish if it is really hypocalcaemia, apparent hypocalcaemia may be an artefact of hypoalbuminaemia

349
Q

3 causes of hypocalcaemia with increased phosphate

A

chronic kidney disease
hypoparathyroidism
pseudohypoparathyroidism

350
Q

3 causes of hypocalcaemia with equal or decreased phosphate

A

vitamin D deficiency
osteomalacia
acute pancreatitis
respiratory alkalosis

351
Q

signs of symptoms of hypocalcaemia

A 
SPASMOC
Spasms - Trousseau's sign 
Paraesthesia 
Anxious
Seizures
Muscle tone increases in smooth muscle 
Orientation is impaired --> confusion 
Chvostek's sign - tap over the facial nerve and look for spasm of facial muscles
352
Q

What abnormality would show on an ECG of hypocalacemia

A

Long QT interval

353
Q

Treatment for mild and severe hypocalcaemia

A

mild : give calcium and check daily plasma Ca2+

severe : calcium gluconate IV over 30 mins

354
Q

briefly outline the physiology of calcium homeostasis

A
  • decreased in serum Ca2+
  • stimulates an increase in parathyroid hormone
  • PTH leads to: bone resorption, and Ca2+ resorption at the kidney and intestine to increase serum calcium
355
Q

what is the set point of ionised calcium

356
Q

2 causes of hypercalcaemia

A

Malignancy - bone mets, myeloma, lymphoma

Primary hyperparathyroidism

357
Q

symptoms of hypercalcaemia

A

bones, stones, moans and psychic groans

  • bone ache and pain
  • renal stones
  • abdominal pain, vomiting, constipation
  • confusion
358
Q

aims of the investigations for hypercalcaemia

A

need to distinguish if it is malignancy or primary hyperparathyroidism

359
Q

what results point towards malignancy as a causes for hypercalcaemia

A

low PTH
high calcium
low phosphate
PTH is appropriate

360
Q

what results point towards hyperparathyroidism as a causes for hypercalcaemia

A

PTH is high (inappropriate)

361
Q

treatment of acute hypercalcaemia

A

correct dehydration
bisphosphonates
(chemo may help in malignancy)

362
Q

What is hyperparathyroidism

A

high levels of PTH

363
Q

physiology of the parathyroid gland

A
  • 4 parathyroid glands in the 4 corners of the thyroid gland
  • chief cells produce PTH in response to low serum ionised calcium conc
  • PTH acts to increased to Ca2+ conc by : increasing absorption from the intestine, increasing reabsorption from the kidneys and increasing the osteoclast activity in the bones
364
Q

cause of primary hyperparathyroidism

A

tumour

usually solitary benign adenoma

365
Q

presentation of primary hyperparathyroidism

A

signs and symptoms of hypercalcaemia

bones, stone, moans and groans

366
Q

what is the PTH and Ca2+ in primary hyperparathyroidism

367
Q

Treatment of primary hyperparathyroidism

A

surgical removal of tumour

368
Q

what are the causes of secondary hyperparathyroidism

A

insufficient vitamin D or chronic renal failure

369
Q

pathogenesis of secondary hyperparathyroidism

A

reduced absorption of calcium (hypocalcaemia)

PT glands secrete PTH to compensate

370
Q

PTH and Ca2+ in secondary hyperparathyroidism

A

PTH : appropriately high

Ca2+ : decreased or normal

371
Q

treatment for secondary hyperparathyroidism

A

increase vitamin D

Kidney transplant

372
Q

what is the pathogenesis of tertiary hyperparathyroidism

A

secondary continues for a long period of time leading to large hyperplasia of the PT glands
causing hypercalcaemia

373
Q

treatment of tertiary hyperparathyroidism

A

surgery to remove PT glands

374
Q

PTH and Ca2+ in tertiary hyperparathyroidism

A

PTH : inappropriately high

Ca2+ : high

375
Q

what is hypoparathyroidism

A

state of decreased secretion or activity of PTH leading to decreased blood levels of calcium and increased levels of phosphate

376
Q

3 causes of hypoparathyroidism

A
  1. surgery
  2. Di George syndrome
  3. Radiation
  4. Autoimmune
377
Q

pathophysiology of hypoparathyroidism

A

decreased PTH
decreased renal calcium reabsorption, increased renal phosphate reabsorption, decreased bone resorption and decreased formation of 1,25(OH)2D
All leads to decreased serum calcium

Phase 2A (11 decks)

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