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CP3 Medicine > Endocrinology p1 > Flashcards

Endocrinology p1 Flashcards

1
Q

What is DM?

A

A multi system disease resulting from inadequate action of the hormone insulin

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2
Q

what is the pathophysiology of T1DM?

A

autoimmune disease with autoantibodies targeted against the insulin secreting beta cells of the pancreas, leading to cell death and inadequate insulin secretion

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3
Q

What is the clinical presentation of T1DM?

A

presents in childhood / adolescence with a 2-6 week history of:
polyuria - high sugar content in urine leading to osmotic diuresis
polydipsia - due to resulting fluid loss
weight loss: fluid depletion plus fat / muscle breakdown

DKA = common first presentation

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4
Q

What is the pathophysiology of T2DM?

A

Insensitivity of body tissues to insulin

‘insulin resistance’

Eventually, Beta cells decompensate and can no longer produce excess insulin, leading to hyperglycaemia

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5
Q

What are the causes of T2DM?

A 
Age
genetic factors
obesity 
high fat diet
sedentary lifestyle
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6
Q

What is the clinical presentation of T2DM?

A

polyuria
polydipsia
weight loss

lack of energy
visual blurring: glucose induced refractive changes
pruritus vulvae / balanitis due to candida

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7
Q

What complications arise as a result of T2dm?

A

retinopathy
polyneuropathy
erectile dysfunciton
arterial disease: MI / peripheral vascular disease

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8
Q

What is the metabolic syndrome?

A

T2DM
central obesity
dyslipidaemia: Low HDL cholesterol, hyptertriglyceridae,ia

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9
Q

What are the secondary causes of T2DM?

A

Pancreatic disease: CF, chronic pancreatitis, pancreatic carcinoma

Endocrine disease: Cushing’s disease, acromegaly, thyrotoxicosis, PCC, glucagonoma

Drug induced: thiazide diuretics, corticosteroids, antipsychotics, antiretrovirals

Congenital disease: insulin receptor abnormalities, myotonic dystrophy, friedreicqh’s ataxia

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10
Q

What are the diagnostic criteria for T2DM?

A

usually diagnosed by Hba1c of 48mmol/mol or more in a symptomatic individual

Assess blood glucose over the last 8-12 weeks

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11
Q

In which populations is HbA1c inappropriate in?

A 
haemoglobinopathies
haemolytic anaemia
untreated iron deficiency anaemia
suspected gestational diabetes
children
HIV
chronic kidney disease
people taking medication that may cause hyperglycaemia (for example corticosteroids)
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12
Q

If you can’t use Hba1c, what is diagnostic of diabetes?

A

Fasting plasma glucose of 7mmol/l or creater

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13
Q

How should diabetes diagnosis be done on an asymptomatic individual?

A

Never be based on a single abnormal HbA1c or fasting plasma glucose - at least 1 additional abnormal Hba1c or plasma glucose level is essential

If the second test results = normal, arrange regular review

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14
Q

What are the normal ranges for fasting and after OGTT?

A

normal: fasting <7mmol/L

2h glucose: <7.8mmol/l

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15
Q

What are the results of impaired glucose tolerance?

A

Fasting <7 and 2h glucose 7.8-11.0mmol/L

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16
Q

What are the results of diabetes mellitus?

A

Fasting glucose >7mmol/L

2h glucose >11.0mmol/L

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17
Q

How is T1DM diagnosed?

A

Random blood glucose of >11.0mmol/L in symptomatic individual

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18
Q

What is the lifestyle management of T2DM?

A

Education
Screen for complications: fundoscopy, nephropathy
first pass morning urine for albumin:creatinine
serum creatinine for eGFR

Foot check: neuropathy, ischaemia, ulcers, deformity

Monitor CV risk: control blood pressure
Assess Qrisk2 score: atorvastatin for those >10%

Lifestyle advice: diet

Weight loss

Exercise: 20-30mins/day

Stop smoking

Alcohol reduction

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19
Q

What dietary advice is given in T2DM?

A

High in low GI carbohydrates
limit foods high in sugar and saturated fats
diabetic specific foods not required
can see nutritionist to help with meal plans

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20
Q

What is the HBA1c target for T2DM?

A

6.5% or 48mmol/L is the target HbA1c initially

53mmol/L = target for all patients on insulin / taking a drug associated with hypoglycaemia

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21
Q

At what level for HbA1c should you start drug treatment?

A

58mmol/mol or higher

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22
Q

What should be offered as the first drug in T2DM?

A

Biguanide such as standard release metformin unless contra-indicated (creatinine clearance below 60) titrated upwards (overweight)

Sulphonylurea in underweight

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23
Q

What dose of metformin should be given initially?

A

500mg with breakfast for one week
500mg with breakfast and dinner for one week
500mg with breakfast, lunch and dinner thereafter

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24
Q

What should be given if metformin is not tolerated or contra-indicated?

A

A gliptin (DPP-4 inhibitor): sitagliptin, lanagliptin

A thiazolidinedione (PPAR-Gamma activator: pioglitazone

A sulphonylurea: gibenclamide, gliclazide

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25
Q

What if metformin alone is not effective?

A

Metformin and one second drug

If metformin contraindicated - any two of the drugs listed above

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26
Q

What if combination therapy is not effective?

A

Triple therapy:
metformin
a sulphonylurea
A gliptin / pioglitazone

If metformin contra-indicated, consider insulin regimens

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27
Q

Give an example of a biguinaide?

A

Metformin

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28
Q

How do biguinaides work?

A

Decrease hepatic glucose production and increase peripheral insulin sensitivity
(do not pose a risk of hypoglycaemia when used as mono therapy)

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29
Q

What level of renal function is needed at least, in order to start metformin treatment?

A

Do not start if eGFR is less than 30mL/min/1.73m2

Review the dose if it is less than 45

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30
Q

What are the contraindications of metformin?

A

eGFR <30 for standard release or <45 for modified release
alcohol addiction
people at risk of lactic acidosis e.g. DKA
People at risk of tissue hypoxia: e.g. cardiac / resp failure

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31
Q

What are the side effects of metformin?

A

GI effects: nausea, vomiting, abdominal pain, loss of appetite
Generally resolve spontaneously

lactic acidosis: rare but serious, occurs due to drug accumulation
insidious onset with non-specific symptoms
more common when combined with alcohol

Vitamin b12 deficiency

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32
Q

Give examples of sulphonylureas

A

Tolbutamide, gliclazide, glibenclamide

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33
Q

How do sulphonylureas work?

A

Increase insulin secretion

Thus only work if some residual function of pancreatic B cells

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34
Q

Which of the sulphonylureas are short, medium and long acting?

A

Tolbutamide = short acting

Gliclazide = medium acting

Glibenclamide = long acting

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35
Q

what is the indication for glibenclamide over the others?

A

if there is a risk of hypoglycaemia

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36
Q

what groups need cautious prescribing for sulphonylureas?

A

elderly: risks of hypoglycaemic events
obese: encourages weight gain

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37
Q

What are the side effects of sulphonylureas?

A

GI disturbances, liver dysfunction

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38
Q

Give examples of thiazolidinediones

A

Pioglitazone

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39
Q

What is the action of a thiazolidinedione?

A

PPAR-Gamma activators - increase peripheral insulin sensitivity

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40
Q

What are the side effects of thiazolidinediones?

A

Weight gain: redistribution of ectopically stored lipid
Fluid retention: contraindicated in CCF
Liver dysfunction: monitor LFTs
Association with bladder cancer: assess risk factors

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41
Q

Give an example of a gliptin

A

Sitagliptin

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42
Q

How do gliptins work?

A

DPP-4 inhibitors, thus increase post-prandial insulin release

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43
Q

In which patients should gliptins be avoided?

A

cardiac, hepatic or renal dysfunction

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44
Q

What are the side effects of gliptins?

A

GI disturbances

rarely - acute pancreatitis

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45
Q

Give an example of a GLP-1 mimetic

A

enaxatide

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46
Q

In what circumstances would you give a GLP-1 mimetic?

A

If triple therapy is ineffective, then the gliptin / pioglitazone can be replaced by GLP-1 mimetic if:

Patient has a BMI >35 or
Patient has a BMI <35 and weight loss would benefit other co-morbitidies
insulin therapy would have negative occupational impacts

n.b. given by SC injection

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47
Q

What are the indications for insulin therapy?

A

All patients with T1DM that present below the age of 40 and all patients with T2DM that fail to respond to full medical treatment or are unsuitable for medical treatments

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48
Q

Describe the principles of management of T1DM?

A

Individualised care plan
Structured education programme
DAFNE: dose-adjustment for normal eating

Screen for complications: less common in early onset disease as not enough time to develop

Lifestyle advice:
Diet: carbohydrate counting is the most important advice as taught in DAFNE
Advice for how to adjust diet / insulin for exercise and consuming alcohol

Insulin regimen

Annual review

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49
Q

What are the three types of insulin available in the UK

A

human insulin
human insulin analogues
animal insulin

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50
Q

How is human insulin produced?

A

recombinant DNA technology - and have the exact same amino acid sequence as human insulin

Produced in the same way as human insulin but the insulin is modified to produce a specific desired kinetic characteristic e.g. an extended duration of action or faster absorption

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51
Q

Give examples of rapid acting insulin

A

Novorapid
Humalog
Apidra

These start working after around 10 minutes and last around 4 hours

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52
Q

How are short acting insulins used?

A

Injected with, or after food
Routine use after food should be discouraged
Onset of action = 15 minutes
Duration of action = 2-5 Hours

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53
Q

Give examples of short acting insulin

A

Actrapid
Humulin S
Insuman Rapid

These start working in around 30 minutes and last around 8 hours

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54
Q

How are soluble insulins used?

short acting insulins

A

Generally injected 30 minutes before food
Onset of action 30-60 minutes
Duration of action up to 8 Hours

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55
Q

What are examples of intermediate acting insulins?

A

Insulatard
Humulin I
Insuman Basal

These start working in around 1 hour and last around 16 hours

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56
Q

Give examples of intermediate acting insulins?

A

Humulin I, Insulatard

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57
Q

How are intermediate acting insulins used?

A

Onset of action 1-2 hours
Maximal effects between 4-12 hours
Duration of action up to 16-35 hours

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58
Q

What Is the purpose of long acting insulins?

A

Mimic basal insulin secretion

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59
Q

Give examples of Long acting insulins

A

These starts working in around 1 hour and lasts around 24 hours:

Lantus
Levemir
Degludec (lasts over 40 hours)

60
Q

How are long acting insulins used?

A

Used once/twice per day, achieved a steady state level after 2-4 days

61
Q

What is novomix?

A

Combination insulin - These containing a rapid acting and an intermediate acting insulin.

62
Q

Describe the typical insulin regime for T1DM

A

Basal bolus regimes recommended
Twice daily long-acting insulin: Detemir
Rapid acting insulin with each meal: Novorapid

If this is not possible, twice-daily mixed insulin regimens can be tried
If the patient cannot achieve HbA1c <8.5%, insulin pumps can be considered by a specialist team

63
Q

wHat is the insulin regime for T2DM?

A

Continue metformin treatment to prevent excess weight gain

Intermediate acting insulin injected once/twice daily according to need

Biphasic preparations cane used if patient’s HbA1c is particularly high

64
Q

What considerations are there if there is poor diabetic control on insulin?

A 
Non-adherence to treatment
Poor injection technique 
Non-rotation of injection sites
Inappropriate dose titration
Psychosocial issues
Organic causes (?CKD)
65
Q

What are the complications of insulin therapy?

A

General: weight Gain, avoided by DAFNE
Insulin resistance can develop

At the injection site: Pain, redness, swelling
Injection site abscess
lipohypertrophy:can result in erratic insulin absotrption

66
Q

How is blood glucose monitored on a day to day?

A

Patients are asked to take four finger prick glucose readings on two days each week
Optimal targets are:
fasting: 5-7mmol on waking

Plasma glucose: 4-7 mmol/L before meals at other times of the day

Plasma glucose: 5-9mmol/L 90 minutes after eating

67
Q

What are the sick day rules for diabetes?

A

Do not stop insulin therapy - seek advice from diabetes team on how to adjust insulin doses
monitor blood glucose more frequently: every 3-4 hours including overnight
consider blood/urine ketone monitoring

Maintain normal meal pattern where possible - replace meals with sugary drinks if appetite reduced

Drink at least 3L fluid/day. Seek advice if unable to do this due to nausea/vomiting
IV fluids may be required

68
Q

In what circumstances would a patient need to inform the DVLA about their diabetes?

A

2 episodes of severe hypoglycaemia within the last 12 months
Reduced awareness of hypoglycaemic episodes

They are on insulin therapy

If on insulin, they must test their blood glucose every 2 hours on long journeys and carry appropriate glucose stores in case of hypoglycaemic events

69
Q

What are the essential components of an annual diabetic review?

A 
Assess cardiovascular risk: Macrovascular complications: 
BMI
BP
Smoking
Blood lipid
Microvascular complications: 
History: ED / neuropathic pain 
Foot exam: neurovascular status 
Fundoscopy: retinal involvement 
Urine dip, first pass urine and plasma creatinine: renal involement

Assess diabetic control: Self monitoring and Hba1c

Assess concordance to diet/lifestyle advice
Assess for adverse events: hospitalisation, symptoms of hypoglycaemic episode, medication side effects, injection site reaction

Depression and anxiety

70
Q

What is DKA?

A

Diabetic ketoacidosis

Metabolic emergency in which hyperglycaemia is associated with metabolic acidosis due to greatly raised ketone levels

Associated with T1DM

71
Q

Describe pathophysiology of DKA

A

ABSOLUTE insulin deficiency
Ketoacidosis - uncontrolled catabolism: ketogenesis
higher and higher glucose and ketones levels. Initially the kidneys produce bicarbonate to counteract the ketone acids in the blood and maintain a normal pH, but this is overwhelmed

Dehydration- Hyperglycaemia overwhelms the kidneys and glucose starts being filtered into the urine. The glucose in the urine draws water out with it in a process called osmotic diuresis.

Potassium Imbalance

Insulin normally drives potassium into cells. Without insulin potassium is not added to and stored in cells. Serum potassium can be high or normal as the kidneys continue to balance blood potassium with the potassium excreted in the urine, however total body potassium is low because no potassium is stored in the cells.

72
Q

Describe how renal perfusion is affected in DKA

A

Increased excretion of sodium and potassium
Despite a significant total body deficit of K+, initial serum K+ is typically normal or even elevated (pseudo-hyperkalaemia)

Serum K+ will then usually fall during treatment as the exogenous insulin drives K+ into cells

If serum K+ is not monitored and replaced as needed, life-threatening hypokalaemia may develop

73
Q

Why do you get normal K+ initially in DKA?

A

Extracellular migration of K+ in response to acidosis and insulin deprivation

74
Q

What are the common reasons for DKA development?

A

Previously undiagnosed diabetes
Interruption of insulin therapy
The stress of intercurrent illness/surgery

75
Q

What are the clinical presentations of DKA?

A 
NEED A KFC
N: nausea and vomiting 
E: excessive thirst
E: excessive urination 
D: dehydration

A: Abdominal pain

K: Kussmaul respiration
F: Fruity breath
C: Coma and death

76
Q

How is diagnosis of DKA done?

A

ALL 3 of:
1. Hyperglycaemia (i.e. blood glucose > 11 mmol/l)

  1. Ketosis (i.e. blood ketones > 3 mmol/l)
  2. Acidosis (i.e. pH < 7.3)
77
Q

What are the essential investigations for DKA?

A

U+Es, creatinine, blood glucose
Venous blood gas: arterial puncture not generally required
Metabolic acidosis with raised anion gap

ECG, Chest Xray, cultures, pregnancy test based on clinical suspicion

N.B. raised WCC Is common, as is raised amylase

78
Q

How is severity of DKA determined?

A

Mild: pH >7.3
Moderate: pH 7.1-7.3
Severe: pH <7.1

79
Q

What is the immediate treatment of DKA?

A

ABCDE
+ FIGPICK

F – Fluids – IV fluid resuscitation with normal saline (e.g. 1 litre stat, then 4 litres with added potassium over the next 12 hours)

I – Insulin – Add an insulin infusion (e.g. Actrapid at 0.1
Unit/kg/hour)

G – Glucose – Closely monitor blood glucose and add a dextrose infusion if below a certain level (e.g. 14 mmol/l)

P – Potassium – Closely monitor serum potassium (e.g. 4 hourly) and correct as required

I – Infection – Treat underlying triggers such as infection

C – Chart fluid balance

K – Ketones – Monitor blood ketones (or bicarbonate if ketone monitoring is unavailable)

80
Q

When should critical care review be sought in DKA?

A

Severe DKA, drowsy, pregnant, sats <94% on 40% O2 or persistent hypotension (<90SBP) after 2L of sodium chloride

81
Q

What is the further treatment of DKA?

A

Continue fixed rate insulin at 0.1units/kg/hr and continue normal long acting insulin
Aim for blood glucose fall of >3mmol/L/hour until <14mmol/L
if not glucose is not falling, check dosage, pump operation, patient weight, reassess concomitant illness
Increase rate by 1 unit / hour every hour ifneccessary

Continue IV 0.9% NaCL
When glucose is <14mmol/L add 10% glucose at 125ml/hour

Potassium: if Plasma K <5.4, add 40mmol KCL per litre NaCl
consider after the first litre of fluid has run through

clinically reassess the patient hourly
regular lab monitoring of glucose, ketones, K+ and HCO3 is required

82
Q

How should fluid be given in DKA?

A 
1L STAT. 
First bag: 1L over 1 hour
Second bag: 1L over 2 hours 
Consider KCL from second bag onwards 
Third bag: 1L over 2 Hours 
Fourth bag: 1L over 4 hours
83
Q

How should DKA be managed when the patient has recovered?

A

Transfer to SC insulin once the patient is able to eat and drink normally and venous pH is >7.3

Stop the IV infusion 1 hour after the next SC injection of insulin
Refer all patients to the diabetes team prior to discharge

84
Q

What is HHS?

A

Complication of T2DM:
severe hypergycaemia causes a hyperosmolar state in the absence of severe ketosis
even a small amount of insulin is enough to prevent ketosis

85
Q

What are the precipitants of HHS?

A

Consumption of glucose-rich fluids
Medications: thiazide diuretics, steroids, B-blockers
Intercurrent illness: infection / MI

86
Q

What are the features of HHS?

A

Patients may be more severely dehydrated than DKA patients but there will be no raised ketones
Can be a lactic acidosis, but is generally mild

Features: dehydration, stupor, coma, seizures

Evidence of an underlying illness

87
Q

How is diagnosis of HHS done?

A

Calculating osmolality:

2(Na+) + urea + glucose

88
Q

What is the normal osmolality?

What value suggests HHS?

A

Normal: 280-295

Values >320 suggest HHS

89
Q

What is the management of HHS?

A

Aggressive IV fluids: 1L 0.9% NaCL over 1 hour
Aim for positive balance of 3-6L over 12 hours

Low dose fixed dose IV insulin infusion
If ketones -treat as DKA and start immediately
If no ketones: add insulin once fall in glucose is <5mmol/L/hr

Consider potassium replacement: if 3.5-5.5 - 40mmolL

Regular monitoring

90
Q

How long will normalisation of fluids and electrolytes take in HHS?
How should patients be managed in recovery?

A

may take 72 hours

Transfer to SC insulin when eating and drinking and normal biochemistry
Stop IV infusion 1 hour after starting SC insulin

91
Q

What is hypoglycaemia?

A

Plasma glucose <3mmol/L, but individual thresholds for symptoms are variable

Symptoms are autonomic or neuroglycopenic

92
Q

What are the autonomic symptoms of hypoglycaemia?

A 
Sweating 
Anxiety
Hunger 
Tremor 
Palpitations
93
Q

What are the neuroglycopenic symptoms of hypoglycaemia?

A

Confusion
Drowsiness/Coma
Seizures

94
Q

How does the pancreas react to hypoglycaemia?

A

alpha cells of pancreas will release glucagon, which work to:
increase glycogenolysis
Increase gluconeogenesis
inhibit glycogen synthesis

In T1dm, the alpha cells become insensitive to falls in glucose, thus becoming increasingly vulnerable to hypoglycaemia

95
Q

How does hypoglycaemia occur?

A

Excess insulin:
inhibits hepatic gluconeogenesis and glycogenolysis
either exogenous or insulinoma

Depletion of hepatic glycogen: malnutrition, fasting, exercise or alcohol
liver failure can also cause this

pituitary insufficiency, adrenal insufficiency and non-pancreatic neoplasm can also cause hypoglycaemia

96
Q

What is the management of hypoglycaemia if the patient can swallow?

A

If able to swallow: 10-20g of a fast acting form of carbohydrate: liquid

Recheck blood glucose after 10-15 minutes
should be reversed in 10 minutes

if inadequate response, repeat as above and check again. When symptoms improve, the patient should eat some long acting carbohydrate

97
Q

What is the management of hypoglycaemia If the patient cannot swallow?

A

IM glucagon immediately

If <8 years, 500 micrograms
if >8 years, 1mg

If glucagon not available / person consumed alcohol / patient does not respond - 999

Intake of long acting carb when able to

98
Q

How should hypoglycaemia recovery be managed

A

Vomiting common: precipitate further episodes –> ?hosptial for IV. can also give 20% glucose IV in hospital

Following recovery, never omit insulin in patients with T1DM

99
Q

What is microvascular disease in diabetes?

A

Small vessels of the retina, glomeruli and nerve sheaths are particularly affected

100
Q

What are the different types of diabetic eye disease?

A

Diabetic retinopathy - either proliferative or non-proliferative:
NPDR
PDR (more common in T2DM)

Diabetic maculopathy

CATARACTS

Glaucoma

101
Q

What are the risk factors for diabetic retinopathy?

A

Poor control, smoking, HTN, pregnancy

102
Q

What are the symptoms / signs of NPDR?

A

Usually asymptomatic, and always occurs at some severity after 8-10 years of DM

Features on fundoscopy:
Micro-aneurysms
Exudates: due to leaky vasculature
Haemorrhages: dot, blot, flame shaped

Cotton wool spots (>5 indicated pre-proliferative retinopathy)
Axoplasmic accumulation due to nerve fibre infarcts

Can progress into proliferative

103
Q

What is the Mx of NPDR?

A

good glycemic control

104
Q

What is PDR?

A

Development of new vessels on the optic disc or retina as a response to significant retinal ischaemia

Ischaemia leads to VEGF production

Vessels = fragile and likely to bleed, can give pre-retinal or vitreous haemorrhage

105
Q

What are the symptoms of PDR?

A

Sudden deterioration in acuity

Can also cause AACG due to iris neovasculariasation

106
Q

What is the management of PDR?

A

Laser photocoagulation
Anti-VEGF medications such as ranibizumab and bevacizumab
Vitreoretinal surgery (keyhole surgery on the eye) may be required in severe disease

107
Q

In which type of diabetes is diabetic maculopathy more common?

A

T2DM

108
Q

What is diabetic maculopathy?

A

Specific type of retinopathy that affects the macula

Typically presents as blurring of the vision

109
Q

What are the subtypes of diabetic maculopathy?

A

Focal, diffuse and ischaemic

110
Q

What is the management of diabetic maculopathy?

A

Mx with focal laser to stop focal leaks but mixed maculopathies require more complex treatment

111
Q

What kind of cataracts develop in diabetics?

A

Posterior sub-capsular cataracts

112
Q

Which type of glaucoma is more common in diabetics?

A

Progressive open angle glaucoma

113
Q

What are the neurological complications of DM?

A 
Symmetrical polyneuropathy
Acute painful neuropathy 
Mononeuropathy 
Diabetic amyotrophy
Autonomic neuropathy
114
Q

what is a symmetrical neuropathy?

A

‘glove and stocking’ sensory loss, with vibration, deep pain and temperature lost first

patients complain of losing balance when their eyes are closed e.g. when washing face - decreased proprioception

Walking on cotton wool

Interrosseous wasting of the small mm of feet = foot shape + ulcers

Neuropathic arthropathy can also develop: Charcot’s foot

115
Q

What is acute painful neuropathy?

A

Painful burning in feet, shins and anterior thighs

Associated with poor glycemic control

Typically worse @ night

Usually remits after 3-12 months of good glycemic control

116
Q

What is mononeuropathy?

A

Isolated nerve lesions: E.G.

CN lesions - mainly III, IV and VI: ocular palsies

Isolated peripheral nerve lesions can also occur: e.g. Carpal tunnel syndrome

Foot drop - sciatic nerve

When more than one affected = mono neuritis multiplex

117
Q

What is diabetic amyotrophy?

A

Progressive wasting of muscle tissues
Rare, usually developing in middle aged men
In diabetes, presents as painful wasting of the quadriceps

118
Q

What is autonomic neuropathy?

A

Sympathetic dysfunction leads to postural hypotension, ejaculatory failure, reduced sweating and Horner’s syndrome

Parasympathetic dysfunction leads to erectile dysfunction, constipation, urinary retention and a Holmes-Adie pupil

119
Q

How does diabetes affect the kidneys?

A

Diabetic nephropathy

CKD

120
Q

How should diabetic patients be monitored for renal complications?

A

blood pressure control
test every patient 6 monthly for microalbuminurea i.e. negative urine dip but early morning albumin:creatinine ratio >3

Every patient with microalbuminurea should be started on an ACEi, regardless of blood pressure

121
Q

How does diabetes affect atherosclerosis?

A

Risk factor for atherosclerosis:
2x increased risk of stroke
4x increased risk of MI
50x increased risk of amputation for gangrene

Treatment for DM only has a modest effect on CV risk
Risk are the same as for generalised atherosclerosis in non-diabetics, however are increased with increasing age, increasing duration of symptoms and also in poor control

122
Q

What is a goitre?

A

Painless enlargement of the thyroid gland.

123
Q

What characteristics are described with a goitre?

A

Diffuse vs nodular; pattern of swelling
simple vs toxic: is it actively secreting thyroid hormone
Benign vs malignant

124
Q

What are the ddx for a diffuse goitre?

A 
Physiological - puberty, pregnancy
autoimmune - graves, hashimotos
thyroiditis - subacute, reidel's
endemic - iodine deficiency
drugs - anti-thyroid drugs, lithium, iodine excess amiodarone
125
Q

What are the ddx for a nodular goitre?

A

multinodular: toxic multi nodular goitre, subacute thyroiditis

Solitary nodule: follicular adenoma, benign nodule, thyroid malignancy, lymphoma, metastasis

infiltration (rare): TB, sarcoid

126
Q

Wha investigations should be done for a thyroid swelling?

A

FBC: related anaemia
ESR: may indicate thyroiditis / autoimmune disease
TFTs: TSH, free T4
Thyroid autoantibodies: autoimmune disease
CT neck and thorax (if pressure symptoms)

USS

FNAC if concerned about malignancy

127
Q

What is the management of a goitre

A

Depends on if hyper, hypo or euthyroid

in euthyroid, treatment is not required for a non-malignant nodule unless it is causing pressure symptoms

128
Q

What is thyrotoxicosis?

A

clinical disorder resulting from raised circulating levels of thyroid hormone

Affects 1% of the population
far more common in women 5:1

129
Q

What are the causes of thyrotoxicosis?

A

Grave’s disease:
toxic multi nodular goitre

Solitary toxic adenoma
Thyroiditis 
drug-induced 
excess iodine intake 
hashitoxicosis

Rare - TSH secreting pituitary adenoma
Resistance to thyroid hormone

130
Q

What are the symptoms of hyperthyroidism?

A 
Anxiety/irritability
Heat intolerance/sweating
Increased appetite
Palpitations
weight loss
tremor 
loose motions
fatigue/weakness
131
Q

What are the signs of hyperthyroidism?

A 
lid retraction / lid lag
Graves' ophthalmopathy*
Goitre/bruit*
systolic hypertension 
tachycardia / AF
tremor 
hyper-reflexia
warm peripheries
acropachy*
proximal weakness
pre-tibial myxoedema*
132
Q

What is Graves ophthalmopathy?

A

Inability to close eyes completely
Exophthalmos / proptosis: bulging eyes
ophthalmoplegia - especially affecting upwards and lateral gaze

Periorbital oedema

133
Q

What is a thyroid storm?

A

Rare presentation of hyperthyroidism, in people with untreated disease in periods of stress: infection, surgery, childbirth:

Hyperpyrexia
Severe tachycardia
Profuse sweating
Confusion / psychosis

If untreated, coma and death may ensue

134
Q

What is the treatment of thyroid storm?

A

symptomatic treatment e.g. paracetamol
treatment of underlying precipitating event
beta-blockers: typically IV propranolol
anti-thyroid drugs: e.g. methimazole or propylthiouracil
Lugol’s iodine
dexamethasone - e.g. 4mg IV qds - blocks the conversion of T4 to T3

135
Q

What are the investigations for hyperthyroidism?

A

TSH: fully suppressed - unless in the rare case of pituitary adenoma

Free T3/T4: elevated (typically both but sometimes just T3 and not T4)

TSH receptor antibody: sensitive and specific for graves disease

Technetium uptake scan: can distinguish from Grave’s disease, toxic multinodular goitre, toxic adenoma or thyroiditis

CT/MRI of the orbit:

136
Q

Describe the patterns of uptake of technetium scanning

A

Diffuse pattern of uptake in Graves’ disease
One of more ‘hot’ nodules in toxic multinodular goitre
reduced/absent uptake in thyroiditis

137
Q

What is the management of hyperthyroidism in primary care?

A

B-blocker: 20-40mg tds for rapid relief of symptoms

May be the only treatment required for cases of thyroiditis

Refer to a specialist endocrinologist

138
Q

What is the management of hyperthyroidism in secondary care?

A

Antithyroid drugs, radioactive iodine therapy, or surgical management for Grave’s disease

1st line: CARBIMAZOLE
2nd line: Propylthiouracil

Block and replace
High dose and titrate down until the patient is euthyroid

RAI or surgical management for other pathologies

139
Q

What is the first line antithyroid drug?

A

Carbimazole

then Propylthiouracil

140
Q

How do antithyroid drugs use?

A

Act as Preferred substate for thyroid peroxidase, the key enzyme in thyroid hormone synthesis

141
Q

What are the side effects of anti-thyroid drugs?

A

Skin rashes
agranulocytosis/thrombocytopenia

Carbimazole can cause cholestatic jaundice

142
Q

Describe the uses of RAI therapy?

A

Used first line in non-Grave’s pathology, or following failure of drug therapy in Grave’s

Taken up by thyroid cells and induces DNA damage and cell death

143
Q

How should a patient beginning RAI therapy be counselled?

A

Contraindicated in pregnancy and in active Grave’s ophthalmopathy

Can cause worsening of eye symptoms

Patients should avoid prolonged contact with children for three weeks after treatment and should not attempt to conceive for 6 months

Rarely can cause worsening of symptoms and thyroid storm

Slight increased risk of thyroid acnes

144
Q

What surgeries are done for hyperthyroidism and what are the indications?

A

Total or sub-total thyroidectomy
Indicated if the above measures have failed or are contraindicated
if there is a suspicion of malignancy, or to manage a large toxic goitre

145
Q

What are the post-op complications of thyroidectomy?

A

Haematoma formation causing asphyxia
emergency removal of sutures

Hypothyroidism (10%)
Hypocalcaemia: due to hypoparathyroidism (often transient)

Vocal cord paresis

CP3 Medicine (19 decks)

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