Brainscape's Knowledge GenomeTM

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


See full index

Phase 2a Lecture Notes > Endocrine > Flashcards

Endocrine Flashcards

1
Q

Sources of glucose in fasting state

A

all glucose comes from liver (and a bit from kidney)
Breakdown of glucose- Gluconeogenesis
Glucose is delivered to insulin independent tissues, brain and red blood cells

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

Gluconeogenesis

A

synthesises glucose from lactate, alanine and glycerol- reverse of glycolysis, occur in liver and kidney

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

Insulin levels in fasting states

A

Insulin levels are low

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

Sources of fuel for muscles

A

Muscle uses free fatty acids for fuel

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

Physiological changes after feeding

A

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

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

Site of insulin and glucagon secretion

A

Islet of Langerhans of the pancreas

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

Cell that secrete insulin

A

Beta cells of islet of Langerhans

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

Cell that secrete glucagon

A

Alpha cells of islet of Langerhans

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

Paracrine crosstalk

A

between alpha and beta cells is physiological, ie local insulin release inhibits glucagon an effect lost in diabetes

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

Action of Insulin

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Action of Glucagon

A

Increases hepatic glucose output
-Glycogenolysis
-Gluconeogenesis
Reduce peripheral glucose uptake
Stimulate peripheral release of gluconeogenic precursors (glycerol, AAs)
-Lipolysis
-Muscle glycogenolysis and breakdown

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

Diabetes mellitus

A

A chronic disorder of carbohydrate metabolism characterised by hyperglycaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Type 1 DM- presentations

A

Typically childhood
Commonly present DKA
Polydipsia, Polyuria, Sudden unexplained weight loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Acute hyperglycaemia morbidity

A

If untreated leads to acute metabolic emergencies diabetic ketoacidosis (DKA) and hyperosmolar coma (Hyperosmolar Hyperglycaemic State )

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Chronic hyperglycaemia morbidity

A

Leads to tissue complications (macrovascular and microvascular)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Side effects of DM treatment

A

Hypoglycaemia- can be fatal

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

Diseases associated with DM

A

Stroke
CV disease
Diabetic retinopathy (vision loss), nephropathy, neuropathy (leading to lower extremity loss)

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

DM diagnosis and investigation- symptomatic

A

Raised plasma glucose detected once-
fasting>7mmol/L
random>11.1 mmol/L

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

DM diagnosis and investigation- asymptomatic

A

Raised plasma glucose detected on two separate occasions-
fasting>7mmol/L
random>11.1 mmol/L
or oral glucose tolerance test- fasting>7mmol/L
2 hours after taking glucose >11.1 mmol/L

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

Pathogenesis of Type 1 diabetes

A

Autoimmune disease causing destruction of beat cells. No insulin production, cells cannot take glucose from blood and use it for fuel.
Cell think body is in fasting state, so has no glucose supply. Levels of glucose keep rising leads in to hyperglycaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Type 1 diabetes- failure of insulin secretion

A

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

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

Type 1 diabetes- Failure to treat with insulin

A

Severe insulin deficiency due to autoimmune destruction of the cell lead to hyperglycaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

DKA initial management

A

ABC if unconscious
Replace fluid loss with IV 0.9% saline slowly to avoid cerebral oedema
Replace deficient insulin with insulin (to inhibit ketone production)+ glucose (to prevent hypoglycaemia)
Treat hypokalaemia as a result of therapy if necessary
Treat underlying triggers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Why can insulin treatment for DKA cause hypokalaemia?

A

Insulin decreases potassium levels in the blood by redistributing K+ into the cells via increased sodium-potassium pump activity causing low serum K+ levels— HYPOKALAEMIA

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

Dangers of hypokalaemia

A

Low levels of K+ can cause arrythmia, weakness (as the heart and muscles can struggle to contract)

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

Complications of DKA treatment

A

Cerebral Oedema- due to rapid dilution of high conc salt in blood with IV fluids. This leads to water moving into tissues causing swelling, swelling in the brain can be cause coma/ fatal due to skull being an enclosed space

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

DKA pathophysiology

A
  1. Absence of insulin+
    unrestrained production of glucose + decreased peripheral glucose uptake
  2. Hyperglycaemia+ osmotic diuresis+ dehydration
  3. Peripheral lipolysis, increase free fatty acids, oxidised to acetyl CoA, increased ketone= acidosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

DKA diagnosis

A

Hyperglycaemia (blood glucose >11 mmol/L)
Ketosis (blood ketones> 3 mmol/L)
Acidosis (pH<7.3)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Type 2 diabetes aetiology

A

Impaired Insulin Secretion and Insulin Resistance

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

Type 2 diabetes- impaired insulin action

A

Reduced muscle and fat uptake after eating
Failure to suppress lipolysis and high circulating FFAs
Abnormally high glucose output after a meal

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

Pathogenesis of Type 2 Diabetes- chronic hyperglycaemia

A

Excessive glucose production, more blood in blood, hyperglycaemia, glycosuria

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

Pathogenesis of Type 2 Diabetes- muscle/fat insulin resistance

A

Impaired glucose clearance, less glucose in peripheral tissues, hyperglycaemia, glycosuria

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

Glycosuria

A

the presence of reducing sugars in the urine

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

Principles of treatment of diabetes

A

Control of symptoms
Prevention of acute emergencies, ketoacidosis, hyperglycaemic hyperosmolar states
Identification and prevention of long-term microvascular complications

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

Sulphonylureas

A

work mainly by stimulating beta cells in the pancreas to make more insulin (e.g gliclazide, glibenclamide)

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

Thiazolidinediones

A

Activate genes concerned with glucose uptake and utilisation and lipid metabolism
Improve insulin sensitivity (e.g pioglitazone - ACTOS)

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

GLP-1 action

A

stimulating glucose-dependent insulin release from the pancreatic islets, slows gastric emptying, inhibit inappropriate post-meal glucagon release, and reduce food intake

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

Metformin (biguanide)

A

Best treatment for type 2 diabetes
Reduces rate of gluconeogenesis, so hepatic glucose output decreases, this increases insulin sensitivity
No impact on insulin secretion/ induce hypoglycaemia/ predispose weight gain

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

Type 1 Diabetes

A

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

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

Type 2 Diabetes

A

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

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

Modern insulin therapy in T1D

A

Separation of basal from bolus insulin to mimic physiology

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

T1D treatment-Basal insulin

A

control blood glucose in between meals and particularly during the night
Given once or twice a day

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

T1D treatment-Bolus insulin

A

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

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

T1D treatment-Basal vs Bolus insulin

A

Basal- base level of insulin
Bolus- simulates insulin increase after eating

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

T2D- needing insulin duration of diabetes

A

Year 0- 0% needing insulin
Year 5- 20% needing insulin
Year 10- 50% needing insulins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Basal insulin in type 2 diabetes- Pros

A

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

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

Basal insulin in type 2 diabetes- Cons

A

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

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

Limited role for pre-mixed insulin in diabetes- pros

A

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

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

Limited role for pre-mixed insulin in diabetes- cons

A

Not physiological
Requires consistent meal and exercise pattern
Cannot separately titrate individual insulin compononents

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

Limited role for pre-mixed insulin in diabetes- risks

A

Increased risk for nocturnal hypoglycaemia2,3
Increased risk for fasting hyperglycaemia if basal component does not last long enough

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Best treatment for T1D

A

Intensive basal-bolus insulin therapy

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

Hypoglycaemia

A

low blood glucose levels

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

Level 1 (alert level) hypoglycaemia

A

Plasma glucose <3.9 mmol/l (70 mg/dl) and no symptoms

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

Level 2 (serious biochemical) hypoglycaemia

A

Plasma glucose <3.0 mmol/l 55 mg/dl)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Non-severe symptomatic hypoglycaemia

A

Patient has symptoms but can self-treat and cognitive function is mildly impaired

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Severe symptomatic hypoglycaemia (Level 3)

A

Patient has impaired cognitive function sufficient to require external help to recover

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Hypoglycaemia- pathophysiology brain

A

Cognitive dysfunction
Blackouts, seizures, comas, Psychological effects

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

Hypoglycaemia- pathophysiology heart

A

Increased risk of myocardial ischaemia, Cardiac arrhythmias

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

Hypoglycaemia- pathophysiology musculoskeletal

A

Falls, accidents, driving accidents, Fractures, Dislocations

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

Hypoglycaemia- pathophysiology heart

A

Inflammation, Blood coagulation abnormalities, Haemodynamic changes, Endothelial dysfunction

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

Common hypoglycaemia symptoms- autonomic

A

Trembling, palpitations, sweating, anxiety, hunger

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Common hypoglycaemia symptoms- neuroglycopenic

A

difficulty concentrating, confusion, weakness, drowsiness, dizziness, vision changes, difficulty speaking

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

Common hypoglycaemia symptoms- non specific

A

Nausea, headache

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

Treatment of non severe hypoglycaemia

A

Carbohydrate

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

Normal physiological responses preventing hypoglycaemia at 4.6 mmol/L

A

Inhibition of endogenous insulin secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Normal physiological responses preventing hypoglycaemia at 3.8 mmol/L

A

Glucagon

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

Normal physiological responses preventing hypoglycaemia at 3.6 mmol/L

A

Adrenaline

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

Impaired response to hypoglycaemia

A

No glycogen release, adrenaline is released at 2.5 mmol/L
Altered thresholds lead to impaired awareness and increased risk of severe hypoglycaemia

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

Causes of hypoglycaemia

A

Long duration of diabetes, Tight glycaemic control with repeated episodes of non severe hypoglycaemia, increased age, use of drugs, sleeping, increased physical activity

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

Screening for risk of severe hypoglycaemia

A

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

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

Strategies to prevent hypoglycaemia- patient education

A

Discuss hypoglycaemia risk factors and treatment with patients on insulin or sulphonylureas
Educate patients and caregivers on how to recognize and treat hypoglycaemia
Instruct patients to report hypo episodes to their doctor/educator

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

Treatment of hypoglycaemia

A

Recognize, confirm, treat, retest, eat

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

Treatment of hypoglycaemia- recognize

A

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

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

Treatment of hypoglycaemia- Confirm

A

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

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

Treatment of hypoglycaemia- Treat

A

Treat with 15g fast-acting carbohydrate to relieve symptoms

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

Treatment of hypoglycaemia- Retest

A

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

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

Treatment of hypoglycaemia- Eat

A

Eat a long-acting carbohydrate to prevent recurrence of symptoms

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

Complications of DM- microvascular

A

Peripheral Neuropathy, Retinopathy, Nephropathy

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

Complications of DM- macrovascular

A

Stroke, hypertension, peripheral artery disease, coronary artery disease

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

Parathyroid hormone action- bone

A

increased bone resorption
inhibits osteoblast activity and stimulates osteoclast activity leading to bone breakdown and calcium release

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

Parathyroid hormone action- kidney

A

Increased Ca2+ reabsorption and 1 α - hydroxylation of 25-OH vit D, decreased phosphate reabsorption

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

Parathyroid hormone action- small intestine

A

No direct effect on small intestine however increase Ca2+ absorption because of increased 1,25 (OH) 2 vit D

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

PTH response to decreased serum calcium

A

Decreased serum Ca2+ detected, increased in PTH causes increased Bone resorption and Ca2+ reabsorption in the kidney.
PTH causes decrease of phosphate in the kidneys causing increased urinary phosphate excretion and decrease serum phosphate, resulting in increased 1,25-(OH)2 vit D so increased Ca2+ absorption from the small intestine

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

Ca2+ homeostasis is an example of +ive or -ive feedback

A

negative feedback

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

Does PTH have big or small changes to small changes in serum Ca2+

A

small changes in serum calcium result in big changes in PTH

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

Importance of maintenance of serum Ca2+

A

Functioning of nerves and muscles

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

Hypocalcaemia

A

Low levels of low ionised calcium in the blood

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

Corrected calcium equation

A

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

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

Consequences of Hypocalcaemia

A

Paraesthesia
* Muscle spas (Hands and feet, Larynx, Premature labour)
* Seizures
* Basal ganglia calcification
* Cataracts
* ECG abnormalities- Long QT interval

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

Chvostek’s Sign

A

Tap over the facial nerve
Look for spasm of facial muscles

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

Trousseau’s Sign

A

Inflate the blood pressure cuff to 20 mm Hg above systolic for 5 minutes

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

Causes of Hypocalcaemia

A

Vitamin D inadequacy or vitamin D resistance.
Hypoparathyroidism following surgery.
Hypoparathyroidism owing to autoimmune disease or genetic causes.
Renal disease or end-stage liver disease causing vitamin D inadequacy

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

Hypoparathyroidism

A

diminished concentration of PTH in the blood, which causes deficiencies of calcium and phosphorus compounds in the blood

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

Hypoparathyroidism causes

A
  • Syndromes
  • Genetic
  • Surgical
  • Radiation
  • Autoimmune
  • Infiltration
  • Magnesium deficiency
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

Hypoparathyroidism pathology

A

Decreased renal Ca2+ reabsorption (increased Ca2+ excretion), increased renal phosphate reabsorption (increased serum phosphate), decreased bone resorption, decreased formation of 1,25(OH)2D (decreased intestinal Ca2+ absorption)
OVERALL DECREASED SERUM Ca2+

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

Pseudohypoparathyroidism

A

Resistance to parathyroid hormone

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

Pseudohypoparathyroidism symptoms

A
  • Short stature
  • Obesity
  • Round facies
  • Mild learning difficulties
  • Subcutaneous ossification
  • Short fourth metacarpals
  • Other hormone resistance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

Pseudohypoparathyroidism cause

A

Type 1 Albright hereditary osteodystrophy
– mutation with deficient Gα subunit

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

Pseudohypoparathyroidism pathology

A

= PTH resistance
So if Ca2+ decreases, there is no increased bone resorption or no Ca2+ reabsorption/ absorption

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

Hypercalcaemia

A

High levels of low ionised calcium in the blood

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

Hypercalcaemia- reason for false readings

A
  • Tourniquet on for too long
  • Sample old and haemolysed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

Hypercalcaemia: Symptoms

A
  • Thirst, polyuria
  • Nausea
  • Constipation
  • Confusion > coma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

Hypercalcaemia: Consequences

A
  • Renal stones
  • ECG abnormalities- Short QT
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

Causes of hypercalcaemia

A
  • Malignancy- bone mets, myeloma, PTHrP, lymphoma
  • Primary hyperparathyroidism
  • Thiazides
  • Thyrotoxicosis
  • Sarcoidosis
  • Familial hypocalciuric / benign hypercalcaemia
  • Immobilisation
  • Milk-alkali
  • Adrenal insufficiency
  • Pheochromocytoma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

Most common causes of hypercalcaemia

A

Malignancy
Primary hyperparathyroidism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

Consequences of Primary Hyperparathyroidism

A
  • Bones
    -Osteitis fibrosa cystica
  • Osteoporosis
  • Kidney stones
  • Psychic groans
  • confusion
  • Abdominal moans
  • Constipation
  • Acute pancreatitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

Consequences of Primary Hyperparathyroidism rhyme

A

Bones, Stones, Groans, Moans

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

Primary Hyperparathyroidism pathology

A

Increased PTH leads to increased bone resorption, renal Ca2+ reabsorption, Ca2+ absorption
HYPERCALCAEMIA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

Blood supply of anterior pituitary

A

The anterior pituitary has no arterial blood supply but receives blood through a portal venous circulation from the hypothalamus

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

Regulation of the pituitary

A

Growth, thyroid, puberty + fertility, steroids

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

Location of pituitary gland

A

Sella turcica

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

Structures at risk of enlarged pituitary gland

A

Optic chiasm, contents of cavernous sinus (CN III, CN IV, V1, V2, CN VI + internal carotid artery)

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

Thyroid axis

A

Hypothalamus produces TRH, causes pituitary gland to release TSH, causes thyroid to produce T4 +T3. T4 + T3 causes negative feedback loop and decrease in TRH and TSH production

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

Pituitary problem impact on thyroid axis

A

TSH, T4 and T3 are low and TRH is high

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

Gonadal Axis

A

Hypothalamus produces GnRH, causes pituitary gland to release LH and FSH, causes testes/ ovaries to produce testosterone/ oestrogen. Testosterone/ oestrogen causes negative feedback loop and decrease in GnRH, LH and FSH production

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

HPA Axis

A

Hypothalamus produces CRH, causes pituitary gland to release ACTH, causes adrenal glands to produce cortisol. Cortisol causes negative feedback loop and decrease in CRH and ATCH.

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

GH / IGF-I AXIS

A

Hypothalamus produces GHRH to simulate release of GH from the pituitary gland or SMS to inhibit GH release. GH acts on liver and produces IGF-I. IGF-I causes negative feedback loop.

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

Diseases of the pituitary

A
  • Benign pituitary adenoma
  • Craniopharyngioma
  • Trauma
  • Apoplexy / Sheehans
  • Sarcoid / TB
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

Craniopharyngioma

A

Epithelial tumours located near pituitary gland, extending to involve the hypothalamus, optic chiasm, cranial nerves, third ventricle, and major blood vessels

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

What’s the difference between a craniopharyngioma and a pituitary adenoma?

A

Craniopharyngiomas and pituitary adenomas can both affect hormone function.
-Pituitary adenomas come from your pituitary gland
-craniopharyngiomas are located near that gland

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

Causes of Presentation of pituitary gland tumour

A

Pressure on local structure, pressure on normal pituitary and functioning tumours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

Symptoms causes by pituitary tumour pressing on local structures

A
  • Bitemporal hemianopia
  • Headaches (stretching dura or hydrocephalus)
  • Carinal nerve palsy and temporal lobe epilepsy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

Prolactinomas symptoms

A
  • More common in women
  • Present with galactorrhoea/ amenorrhoea/ infertility
  • Loss of libido
  • Visual field defect
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

Amenorrhoea

A

absence of menstrual periods

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

Galactorrhoea

A

a milky nipple discharge unrelated to the usual milk production of breastfeeding

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

Prolactinomas treatment

A

Treatment dopamine agonist eg Cabergoline or bromocriptine

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

Prolactinomas- 1st line investigations

A

Elevated serum prolactin
Pituitary MRI

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

Prolactinomas

A

Noncancerous tumour of the pituitary gland. This tumour causes the pituitary gland to make too much prolactin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q

Acromegaly

A

Hormonal disorder that develops when your pituitary gland produces too much growth hormone during adulthood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
130
Q

At which stage does pitiuarty tumours cause Acromegaly, not Gigantism

A

Fusion of the long bone epiphysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
131
Q

Cushing syndrome

A

disorder that occurs when your body makes too much of the hormone cortisol over a long period of time

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

Cushing syndrome symptoms

A

Weight gain in the trunk+ face, with thin arms and legs.
A fatty lump between the shoulders
Pink or purple stretch marks
Thin, frail skin that bruises easily
Slow wound healing
Acne

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

Most common causes of Cushing syndrome

A

long-term, high-dose use of the cortisol-like glucocorticoids

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

Do benign pituitary tumours affect anterior or posterior pituitary

A

Anterior pituitary

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

Definitive signs of female puberty

A

Menarche – first menstrual bleeding

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

Definitive signs of male puberty

A

First ejaculation, often nocturnal

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

Secondary sexual characteristics that occur at puberty- female

A

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

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

Secondary sexual characteristics that occur at puberty- male

A

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

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

Tanner stages

A

Scale of physical development based on external primary and secondary sex characteristics

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

Adrenarche

A

developmentally programmed peri-pubertal activation of adrenal androgen production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
141
Q

Pubarche

A

Most pronounced clinical result of adrenarche
* Result of androgen action on the pilosebaceous unit transforming vellus hair into terminal hair in hair-growth prone parts of the skin

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

PRECOCIOUS PUBERTY

A

when children’s bodies begin to change into adult bodies too soon

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

True PRECOCIOUS PUBERTY

A

Early activation of all of the HPG axis, 90% female

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

True PRECOCIOUS PUBERTY differential diagnosis

A

Brain tumour, especially in boys

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

PRECOCIOUS PSEUDOPUBERTY

A

GnRH-independent and occurs due to excess production of sex hormones either from the gonads, the adrenal glands or secreting tumours, HPG axis is not active

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

PRECOCIOUS PUBERTY – TREATMENT

A

Treatment with GnRH super agonist to suppress pulsatility of GnRH secretion

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

Causes of True Precocious Puberty

A

Idiopathic, CNS tumour/disorder, secondary central precocious puberty, psychosocial

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

Causes of Precocious Pseudo-Puberty

A

Increases androgen secretion, gonadotropin secreting tumour, ovarian cyst

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
149
Q

Indication of delayed puberty

A

Girls- lack of breast development by 13
Boys- lack of testicular enlargement by age 14

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
150
Q

CONSTITUTIONAL DELAY OF GROWTH AND PUPERTY (CDGP)

A

Children experience delayed puberty compared to their peers of similar age associated with a delay in the pubertal growth spurt

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

CONSTITUTIONAL DELAY OF GROWTH AND PUPERTY RFs

A

Family history of delayed puberty, congenital pituitary abnormalities, gene mutations, malnutrition, congenital and acquired gonadal abnormalities

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

Primary Hypogonadism

A

Testis/ovaries fail
-Hypergonadotropic and Hypogonadism
-Testosterone/ oestrogen go down, lack of feedback, FSH and LH go up

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

Secondary/Tertiary Hypogonadism

A

Hypothalamus/ Pituitary fail
-Hypogonadotropic and Hypogonadism
- FSH and LH go down, no response to feedback feedback, Testosterone/ oestrogen go down

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
154
Q

Klinefelter’s syndrome

A

Affects males, 47,XXY Primary hypogonadism

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

Turner’s syndrome

A

Affects girls, 45,X0, Hypergonadotropic hypogonadism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
156
Q

Turner’s syndrome- characteristics

A

Short stature, Short neck with a webbed appearance, low hairline at the back of the neck, low-set ears, hands and feet that are swollen or puffy at birth, and soft nails that turn upward

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

Klinefelter’s syndrome- characteristics

A
  • Azoospermia, Gynaecomastia
  • Reduced secondary sexual hair
  • Osteoporosis
  • Tall stature
  • Reduced IQ in 40%
  • 20-fold increased risk of breast cancer
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
158
Q

Hormone replacement therapy- female puberty

A

Low doses of (Ethinyl estradiol (tablet) or Oestrogen (tablets, transdermal)) and gradual increasing doses to provide time for pubertal growth until full adult dose is achieved, then progesterone is added

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

Where is vasopressin and oxytocin made and where is it released from?

A

Made in PVN (paraventricular nucleus) and SON (supraoptic nucleus) transported to the posterior pituitary in the axoplasm of the neurons

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

Osmoreceptors

A

maintain the osmolality of the blood through a coordinated set of neuroendocrine, autonomic, and behavioral feedbacks

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

Arginine Vasopressin (AVP or ADH) release controlled by

A

osmoreceptors in hypothalamus - day to day
baroreceptors in brainstem and great vessels - emergency

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

ECF ions

A

large amounts of sodium, chloride, and bicarbonate ions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
163
Q

ICF ions

A

potassium, magnesium and phosphate ions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
164
Q

Sodium concentration ([Na+]) and ECF osmolarity

A

considered together because sodium ions comprise the majority of the solute in the extracellular compartment

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

Water balance is regulated by a feedback loop: water excess

A

Ingestion of water, decrease Plasma osmolality, increase in cellular hydration, decrease in thirst, vasopressin secretion + water intake, increase in urine excretion, decrease in total body water

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

Water balance is regulated by a feedback loop: water deficit

A

Water loss, increase Plasma osmolality, decrease in cellular hydration, increase in thirst, vasopressin secretion + water intake, decrease in urine excretion, increase in total body water

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

Under normal conditions what mediates variable water excretion by the kidneys

A

Vasopressin

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

Osmolality

A

Concentration in plasma (mOsmol/kg), number of (not size of) particle

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

Serum osmolality equation

A

serum osmolality = 2(Na) + glucose/18 + Urea/2.8

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
170
Q

AVP deficiency (cranial diabetes insipidus)

A

Lack of vasopressin, uncommon not life threating

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
171
Q

AVP resistance (nephrogenic diabetes insipidus)

A

Resistance to action of vasopressin, uncommon not life threating

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

Syndrome of anti-diuretic hormone secretion – SIAD

A

Too much vasopressin release when it should not be released, common, and can be life threatening

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

AVP deficiency and resistance symptoms

A

polyuria (wee), polydipsia (excess thirst), no glycosuria (decreased glucose in urine)

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

AVP deficiency and resistance investigations

A

Measure urine volume - unlikely if urine volume <3L/day
Check renal function and serum calcium

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

AVP deficiency and resistance- diagnostic investigation

A

Water deprivation test

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
176
Q

AVP resistance (nephrogenic DI) causes

A

Genetic disorders,
-acquired: either reduction in medullary concentrating gradient or antagonism of effects of AVP

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

AVP deficiency (Cranial DI) causes

A

Damage to the hypothalamus or pituitary gland – ie after an infection, operation, brain tumour or head injury
Or genetic/ idiopathic (often autoimmune)

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

Management of AVP deficiency (Cranial DI)

A

Treat underlying condition, desmopressin, high activity at V2 receptor

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

Management of AVP resistance (Nephrogenic DI)

A

-try and avoid precipitating drugs
-congenital DI - very difficult
free access to water
very high dose desmopressin

180
Q

Hyponatraemia

A

serum sodium < 135 mmol/l

181
Q

Biochemically serve hyponatremia

A

serum sodium < 125 mmol/l

182
Q

Normal serum sodium

A

135-144mmol

183
Q

Moderate symptoms of Hyponatraemia

A

Headache
Irritability
Nausea / vomiting
Mental slowing
Unstable gait / falls
Confusion / delirium
Disorientation

184
Q

Severe symptoms of Hyponatraemia

A

Stupor / coma
Convulsions
Respiratory arrest

185
Q

Hyponatremia and the brain

A

The brain undergoes volume adaptation in response to gradual-onset hyponatraemia

186
Q

Acute or chronic hyponatremia

A

Acute < 48 hours
Chronic > 48 hours

187
Q

Aetiology of hyponatremia

A

Hypovolaemic
Euvolemic (blood)
Hypervolaemic

188
Q

General Hyponatraemia treatments

A

Stop hypotonic fluids- fluid restriction
Review drug card – long list - PPI etc.

189
Q

Hyponatraemia causes- dehydration + low urine Na+< 20mmol/l

A

Vomiting and diarrhoea
Burns
Pancreatitis
Sodium depletion after diuretics
Saline replacement

190
Q

Hyponatraemia causes- dehydration + high urine Na+>40 mmol/l

A

Diuretics
Addison’s (or occasionally pituitary failure)
Cerebral salt wasting
Salt wasting nephropathy
Saline replacement

191
Q

Hyponatraemia causes- fluid overload

A

Cirrhosis of liver/liver failure
CCF
Inappropriate IV fluids
Fluid restrict

192
Q

SIAD - syndrome of antidiuresis

A

Too much AVP, when it should not be being secreted

193
Q

SIAD- causes

A

Malignancy, primary brain injury (meningitis, bleed), drugs, infections

194
Q

Biochemistry of SIAD - syndrome of antidiuresis

A

Low osmolality
Plasma sodium is low
Urine is inappropriately concentrated
Water retention - ECF volume increased mildly
Increase GRF - less Na reabsorption in PCT
thus - urine Na+ usually >30mmol/l
normal thyroid and adrenal function

195
Q

Treatment goals of SIAD

A

allow/facilitate increase in serum Na+
treat any underlying condition
in acute setting - daily U+E - hospital
in chronic setting - weekly to monthly U+E - hospital/GP

196
Q

Most common causes of hyperthyroidism

A

Graves diseases
Toxic multinodular goitre
Toxic adenoma

197
Q

Goitre

A

Palpable & visible thyroid enlargement
Commonly sporadic or autoimmune

198
Q

Name a disease that is Endemic in iodine deficient areas

A

Goitre

199
Q

SPORADIC NON-TOXIC GOITRE

A

Commonest endocrine disorder
An enlargement of the thyroid gland in a euthyroid subject living in an iodine-sufficient area

200
Q

3 mechanisms for Hyperthyroidism

A

a. overproduction thyroid hormone
b. leakage of preformed hormone from thyroid
c. ingestion of excess thyroid hormone

201
Q

Hyperthyroidism

A

excess of thyroid hormones in blood

202
Q

DRUG INDUCED HYPERTHYROIDISM

A

Iodine
Amiodarone (antiarrhythmic drug)
Lithium
Radiocontrast agents

203
Q

CLINICAL FEATURES of hyperthyroidism

A

Weight loss
Tachycardia +/ AF
Hyperphagia (very hungry)
Anxiety
Tremor
Heat intolerance
Sweating
Diarrhoea
Lid lag + stare
Menstrual disturbance

204
Q

GRAVES’ SPECIFIC clinical features

A

Diffuse goitre
Thyroid eye disease (infiltrative)
Pretibial myxoedema
Acropachy

205
Q

Investigations of hyperthyroidism

A

Thyroid function tests to confirm biochemical hyperthyroidism
Diagnosis of underlying cause important because treatment varies
Clinical history, physical signs usually sufficient for diagnosis

206
Q

Investigations of primary hyperthyroidism- thyroid functions test

A

Increase free T4 + T3
Suppressed TSH

207
Q

Investigations of secondary hyperthyroidism- thyroid functions test

A

Increase free T4 +T3
But inappropriately high TSH

208
Q

If thyroid function test shows high T4+T3, but low TSH, what is the likely diagnosis

A

Graves disease- thyroid function test

209
Q

Graves disease

A

Immune system disorder that results in the overproduction of thyroid hormones (hyperthyroidism)

210
Q

Thyroiditis

A

Inflammation of the thyroid gland

211
Q

Treatment for destructive thyroiditis

A

Antithyroid drugs (course or long-term)
Radioiodine 131I
Surgery (partial, subtotal thyroidectomy)

212
Q

Thionamides

A

Drug class that decreases synthesis of new thyroid hormone

213
Q

SIDE EFFECTS OF THIONAMIDES

A

Generally well tolerated
Common side effect:
rash
Less common:
arthralgia
hepatitis
neuritis
thrombocytopenia
vasculitis

214
Q

Dangerous side effect of thionamides

A

AGRANULOCYTOSIS (destruction of WBCs)

215
Q

Radioiodine mechanism

A

Emission of beta particles results in ionization of thyroid cells
Direct damage to DNA and enzymes
Indirect damage via free radicals

216
Q

Surgical treatment for graves disease and multinodular goitre

A

Near total thyroidectomy for Graves’ disease and multinodular goitre

217
Q

Surgical treatment for toxic adenoma

A

Near total thyroidectomy / lobectomy for toxic adenoma

218
Q

HYPOTHYROIDISM

A

Thyroid hormones levels abnormally low

219
Q

3 types of hypothyroidism

A

PRIMARY (>99%)
- absence / dysfunction thyroid gland
- most cases due to Hashimoto’s thyroiditis
SECONDARY / TERTIARY
- pituitary / hypothalamic dysfunction

220
Q

Causes of primary HYPOTHYROIDISM - ADULT

A

Hashimoto’s thyroiditis
131I therapy
Thyroidectomy
Postpartum thyroiditis
Drugs
Thyroiditides
Iodine deficiency
Thyroid hormone resistance

221
Q

Postpartum thyroiditis

A

Transient phenomenon observed following pregnancy
May cause hyper/hypothyroidism
Often misdiagnosed as postpartum depression

222
Q

Hashimoto’s thyroiditis

A

Autoimmune thyroiditis that produces atrophic changes with regeneration, leading to goitre formation
More common in late middle aged women
Common cause of hypothyrodism

223
Q

Causes secondary/tertiary HYPOTHYROIDISM - ADULT

A

Pituitary disease
Hypothalamic disease

224
Q

Clinical features of hypothyroidism

A

Fatigue
Wt gain
Cold intolerance
Constipation
Menstrual disturbance
Muscle cramps
Slow cerebration
Dry, rough skin
Periorbital oedema
Delayed muscle reflexes
Carotenaemia
Oedema

225
Q

Investigation for primary hypothyroidism

A

high TSH (most sensitive marker)
usually low free T4 + T3

226
Q

Investigations for SECONDARY/TERTIARY HYPOTHYROIDISM

A

TSH inappropriately low for reduced T4 / T3 levels

227
Q

Investigation for Hasimoto’s

A

T4/ T3 may be low/normal in mild hypothyroidism positive titre of TPO antibodies in Hashimoto’s

228
Q

Treatment for hypothyroidism

A

Replacement therapy- synthetic L-thyroxine (T4)

229
Q

Human chorionic gonadotrophin hormone (hCG)

A

hormone produced by the placenta during pregnancy.
It helps thicken uterine lining to support a growing embryo and stops menstruation

230
Q

Metabolic Changes in pregnancy

A

Increased erythropoetin, cortisol, noradrenaline
High cardiac output
Plasma volume expansion
High cholesterol and triglycerides
Pro thrombotic and inflammatory state
Insulin resistance

231
Q

Gestational Syndrome

A

specific to being pregnant

232
Q

Gestational Syndrome examples

A

Pre-Eclampsia
Gestational Diabetes
Obstetric cholestasis
Gestational Thyrotoxicosis
Transient Diabetes Insipidus
Lipid disorders
Postnatal depression
Postpartum thyroiditis
Postnatal autoimmune disease
Paternal Disease

233
Q

Thyroid gland development

A

Foetal thyroid follicles and thyroxine synthesis occurs at 10 weeks
Axis matures at 15-20 weeks
Maternal T4 0-12 weeks regulates neurogenesis, migration and differentiation then foetal T4

234
Q

What week does Fetal thyroid follicles and thyroxine synthesis occur

A

Week 10

235
Q

What weeks does the fetal thyroid axis mature

A

Weeks 15-20

236
Q

Hypothyroidism in pregnancy signs and symptoms

A

Weight gain, cold intolerance, poor concentration, poor sleep pattern, dry skin, constipation, tiredness
Symptoms can predate pregnancy

237
Q

Prevalence of hypothyroidism during pregnancy

A

2-3%

238
Q

hCG and Thyroxine

A

hCG can bind to the TSH receptors present in thyroid tissue and act like a weak form of TSH to cause the thyroid to produce and release more T3 and T4

239
Q

Do expecting mother with hypothyroidism need an increase or decrease in thyroxine dosage

A

Increase as hCG acts of a weak form of TSH causing competition at the receptors

240
Q

Target screening for hypothyroidism

A

Age >30
BMI >40
Miscarriage preterm labour
Personal or family history
Goitre
Anti TPO
Type 1 DM
Head and neck irradiation
Amiodarone, Lithium or contrast use

241
Q

Craniopharyngioma

A

Arise from squamous epithelial remnants of Rathke’s pouch
Benign tumour although infiltrates surrounding structures (pituitary gland and the hypothalamus)

242
Q

LIMITS (not targets) for NA+ rise for hyponatremia treatment

A

High risk- <8mmol/l in any 24 hour period
Normal- <10-12mmol/l in any 24 hour period

243
Q

SIAD - management

A

-Diagnose and treat underlying condition
-fluid restriction <1L/24 hour
-sometimes demeclocycline/ vaptan (vasopressin receptor antagonist)

244
Q

Risk factor for Osmotic Demyelination Syndrome

A

Serum Na+ <105mmol/L
Hypokalaemia
Chronic excess alcohol
Malnutrition
Advanced Liver disease
>18mmol/L Na+ increase in 48 hour

245
Q

Risk of improper therapy for hyponatraemia

A

Rapid correction of the hypotonic state leads to central pontine myelinolysis (osmotic demyelination syndrome)

246
Q

Central pontine myelinolysis (Osmotic demyelination syndrome)

A

Massive demyelination of descending axons
May take up to 2 weeks to manifest

247
Q

Management of acute severe symptomatic hyponatraemia

A
  1. iv 150ml of 3% Saline or equivalent over 20 mins
  2. Check serum Na+
  3. Repeat twice twice until 5mmol/L increase Na+
  4. After 5mmol/L increase
    Stop hypertonic saline
    Establish diagnosis
    Na+ 6 hourly for 1st 24 hours
    Limit increase to 10mmol/l first 24 hour
248
Q

Craniopharyngioma peak ages

A

5 to 14 years; 50 to 74 years

249
Q

Craniopharyngioma symptoms

A

Raised ICP, visual disturbances, growth failure, pituitary hormone deficiency, weight increase

250
Q

Rathke’s pouch

A

gives rise to the anterior pituitary during week 4

251
Q

Rathke’s Cyst

A

Derived from remnants of Rathke’s pouch
Single layer of epithelial cells with mucoid, cellular, or serous components in cyst fluid

252
Q

Rathke’s Cyst symptoms

A

Mostly asymptomatic and small
Present with headache and amenorrhoea, hypopituitarism and hydrocephalus

253
Q

Meningioma symptoms

A

Associated with visual disturbance and endocrine dysfunction
Usually present with loss of visual acuity, endocrine dysfunction and visual field defects

254
Q

Lymphocytic Hypophysitis

A

Inflammation of the pituitary gland due to an autoimmune reaction

255
Q

Non-Functioning Pituitary Adenoma (NFPA) or Silent Pituitary Adenoma (SPA)

A

benign anterior pituitary tumour not associated with clinical evidence of hormonal hypersecretion

256
Q

Non-Functioning Pituitary Adenoma

A

begin tumour can cause visual disturbances, headaches

257
Q

Non-Functioning Tumours

A

No specific test but absence of hormone secretion
* Test normal pituitary function

258
Q

Non-Functioning Tumours treatment

A

Trans-sphenoidal surgery if threatening eyesight or progressively increasing in size

259
Q

Testing Pituitary Function- guiding principle

A

If the peripheral target organ is working normally the pituitary is working

260
Q

Thyroid function test- Primary Hypothyroid

A

Raised TSH low Ft4

261
Q

Thyroid function test-Hypopituitary

A

Hypopituitary - Low Ft4 with normal or low TSH

262
Q

Thyroid function test- Graves disease (toxic)

A

Suppressed TSH high Ft4

263
Q

Thyroid function test- TSHoma- functioning tumour of pituitary (very rare)

A

High Ft4 with normal or high TSH

264
Q

Thyroid function test- Hormone resistance

A

High Ft4 with normal or high TSH

265
Q

Gonadal function test- male- Primary Hypogonadism

A

Low T raised LH/FSH

266
Q

Gonadal function test-male- Hypopituitary

A

Low T normal or low LH/FSH

267
Q

Gonadal function test-male- Anabolic use

A

Low T and suppressed LH

268
Q

Gonadal function test-female- Before puberty

A

Oestradiol very low/undectable with low LH and FSH although FSH slightly higher than LH

269
Q

Gonadal function test-female- Puberty

A

Pulsatile LH increases and oestradiol increases

270
Q

Gonadal function test-female- Post menarche

A

Monthly menstrual cycle with LH/FSH, mid-cycle surge in LH and FSH and levels of oestradiol increase through cycle

271
Q

Gonadal function test-female- Primary ovarian failure (includes menopause)

A

High LH and FSH with FSH greater than LH and low oestradiol

272
Q

Gonadal function test-female- Hypopituitary

A

Oligo or amenorrhoea with low oestradiol and normal or low LH and FSH

273
Q

How to test HPA axis

A

Measure cortisol and synacthen at 0900h

274
Q

HPA function test- Primary AI

A

Low cortisol, high ACTH, poor response to Synacthen

275
Q

HPA function test- Hypopituitarism

A

Low cortisol, low or normal ACTH, poor response to synacthen

276
Q

When is GH levels highest and lowest?

A

GH is secreted in pulses with greatest pulse at night and low or undetectable levels between pulses

277
Q

Affects of obesity on GH

A

Low in obesity

278
Q

Affects of Age on GH

A

falls with age

279
Q

Testing GH/IGF1 axis

A

Measure: IGF-I and GH stimulation test
-Insulin stress test
-Glucagon test

280
Q

How to measure prolactin testing

A

Measure prolactin or cannulated prolactin (3 samples over an hour to exclude stress of venepuncture)

281
Q

Prolactin may be raised as a result of

A

Stress
Drugs: antipsychotics
Stalk pressure
Prolactinoma

282
Q

Measure for pituitary disease

A

Measure Ft4
Measure 0900h fasted T and LH/FSH in pituitary disease

283
Q

Investigation of Vasopressin Deficiency/ Resistance

A

water deprivation test
Hypertonic Saline Stimulation Test

284
Q

Water deprivation test

A

assess the ability of the patient to concentrate urine when fluids are withheld. Water deprivation should normally cause increased secretion of ADH, resulting in smaller volumes of concentrated urine.

285
Q

Hypertonic Saline Stimulation Test

A

technique for distinguishing partial diabetes insipidus from psychogenic polydipsia, and for the diagnosis of complex disorders of osmoreceptor and posterior pituitary function

286
Q

Dynamic Testing

A

assess the dynamic responses of hormonal and metabolic axes. These tests may involve: Stimulation of a hormonal axis by releasing hormones or other agents e.g. Synacthen to stimulate release of cortisol from adrenal glands

287
Q

Preferred imaging study for the pituitary

A

MRI

288
Q

Why is MRI the Preferred imaging study for the pituitary

A

Better visualization of soft tissues and vascular structures than CT
No exposure to ionizing radiation

289
Q

Microparticulate

A

any particle in a micrometer scale are used as drug delivery systems. They offer higher therapeutic and diagnostic performance

290
Q

Thyroxine replacement

A

Aim to achieve levels to mid to upper half of reference range
Higher doses usually required in patients on oestrogens or in pregnancy

291
Q

Growth hormone replacement

A

Aiming for mid-range IGF1 levels, lower doses in older people
Improves lipid profiles, body composition and bone mineral density

292
Q

Testosterone replacement

A

Improve bone mineral density, libido, sexual function, energy levels and sense of well being, muscle mass and reduce fat

293
Q

Oestrogen Replacement

A

Alleviate flushes and night sweats; improve vaginal atrophy
Reduce risk of cardiovascular disease, osteoporosis and mortality

294
Q

Desmopressin replacement therapy

A

Adjust according to symptoms
Monitor sodium levels

295
Q

-Low Ft4 with normal or low TSH
-Low T normal or low LH/FSH
-Low cortisol, low or normal ACTH, poor response to synacthen

A

Hypothyroidism measurement

296
Q

Hypothyroidism measurement

A

-Low Ft4 with normal or low TSH
-Low T normal or low LH/FSH
-Low cortisol, low or normal ACTH, poor response to synacthen

297
Q

Acromegaly mean duration of symptoms

A

8 years

298
Q

Acromegaly mean age at diagnosis

A

44 years

299
Q

Acromegaly Co-morbidities

A

Cerebrovascular events, headaches, arthritis, insulin-resistant diabetes, sleep apnoea, CVD, hypertension

300
Q

Acromegaly presenting clinical symptoms

A

Acral enlargement
Arthralgias
Maxillofacial changes
Excessive sweating
Headache
Hypogonadal symptoms

301
Q

Criteria for diagnosis of acromegaly

A

Acromegaly excluded if:
random GH <0.4 ng/ml and normal IGF-I
If either abnormal proceed to:
75 gm Glucose tolerance test (GTT)
Acromegaly excluded if:
IGF-I normal
and
GTT nadir GH <1 ng/ml

302
Q

Options for treatment of acromegaly

A

Pituitary surgery
Medical therapy
Radiotherapy

303
Q

Two important determinants of success of surgery for acromegaly

A

size of tumour (hence importance of finding early)
surgeon

304
Q

Medical therapy for acromegaly

A

Dopamine agonists – cabergoline
Somatostatin analogues
Growth Hormomne receptor antagonist

305
Q

Mainstay of acromegaly therapy

A

Pituitary surgery mainstay of therapy

306
Q

Prolactinoma

A

Noncancerous tumour of the pituitary gland
Produces prolactin

307
Q

High prolactin levels

A

Reduces the production of the hormones oestrogen and testosterone
Anovulation (prevent release of eggs) in females
Decreased sperm production
Bone loss (osteoporosis)

308
Q

Clinical features of Prolactinoma- local effects of tumour

A

Headache
Visual field defect (bi-temporal hemianopia)
CSF leak (rare)

309
Q

Any pituitary tumour local effect clinical features

A

Headache
Visual field defect (bi-temporal hemianopia)
CSF leak (rare)

310
Q

Clinical features of Prolactinoma- effect of prolactin

A

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

311
Q

Hyperprolactinaemia

A

high prolactin levels

312
Q

Hyperprolactinaemia causes

A

Macroprolactinoma
Microprolactinoma
Non functioning pituitary tumour – compression of pituitary stalk – prolactin <4000 mIU/L
Antidopaminergic drugs
Other causes: stress, hypothyroidism, PCOS, drugs, renal failure, chest wall injury

313
Q

Management of prolactinoma vs other pituitary tumour

A

Unlike other pituitary tumours management is medical rather than surgery

314
Q

Clinical presentation of newly diagnosed
Type 1 diabetes- common

A

2-6 weeks of Polyuria, polydipsia, weight loss, ketonuria (high levels of ketone in urine)

315
Q

Differences between Type 1 and Type 2 diabetes

A

Type 1-immune-mediated, idiopathic, insulin insufficient, younger people
Type 2- insulin resistance with inadequate insulin secretion, result of lifestyle, older people

316
Q

Epidemiology of Type 1 diabetes

A

5-10% of all cases of diabetes, typically present in childhood, however can present later in life

317
Q

Diabetic ketoacidosis (DKA)

A

metabolic emergency in which hyperglycaemia us associated with a metabolic acidosis due to greatly raised ketone levels

318
Q

Diabetic ketoacidosis- ketone levels vs normal

A

> 3mmol/L vs <0.6mmol/L

319
Q

Diabetic ketoacidosis- clinical features

A

Prostration (state of extreme physical exhaustion, weakness or collapse), dehydration, nausea, vomiting
Occasionally- abdominal pain +/ confusion

320
Q

Diabetic ketoacidosis investigation results

A

Ketonemia (>3mmol/L), high blood glucose (>11mmol/L), bicarbonate <15mmol/L +/ venous pH<7.3

321
Q

Diabetic ketoacidosis- treatment

A

Replacement of fluid/ electrolytes lost, restoration of the acid-base balance, insulin replacement, treat underlying cause

322
Q

Diabetic ketoacidosis- pathophysiology- increased glucose

A

Increase glucose due to insulin deficiency >
hyperglycaemia + glycosuria >
osmotic diuresis >
fluid and electrolyte depletion>
renal hypoperfusion >
impaired excretion of ketones + H+

323
Q

Diabetic ketoacidosis- pathophysiology- increased ketones

A

Increase ketones as a result of uncontrolled ketogenesis in the liver due to insulin deficiency > acidosis > vomiting > fluid and electrolyte depletion > renal hypoperfusion > impaired excretion of ketones + H+

324
Q

Aims of treatment of Type 1 diabetes

A

Prevention of diabetes emergencies (ie hypoglycaemia, DKA), Treatment of hyperglycaemic symptoms
Minimise risk of long term complications by screening and control of hyperglycaemia

325
Q

Treatment options in Type 1 diabetes

A

Insulin replacement- pump or injection
Islet cell transplant

326
Q

Monogenic diabetes mellitus (MODY- maturity-onset diabetes of the young)

A

caused by single gene mutation, dominantly inherited, which predominantly affects beta cell function, non-insulin dependence

327
Q

Monogenic vs type 1 diabetes

A

Type 1- doesn’t present before 6 months, immune cell mediated
Monogenic- can affect infants from birth, single genetic cause

328
Q

When to consider monogenic diabetes

A

<6 months, patient presenting with early onset diabetes an affected parent, evidence of non-insulin dependence

329
Q

Secondary diabetes subdivisions

A

secondary to genetic defects beta cell function or insulin action, exocrine pancreatic disease, endocrine disease, drugs/chemicals, infection

330
Q

C peptide

A

Not present in synthetic insulin, longer half life than insulin, type 1 diabetes c-peptide is negative as result of complete destruction of beta cells

331
Q

Will C-peptide persist or disappear with type 1 diabetes?

A

C-peptide will not be present with type 1 diabetes as beta cell are destroyed but will persist for type 1, monogenetic or secondary

332
Q

Secondary diabetes to genetic defects of beta cell function

A

monogenic diabetes, glucokinase/hepatic nuclear factor mutations, neonatal diabetes, mitochondrial diabetes

333
Q

Secondary diabetes to exocrine pancreatic disease causes

A

Chronic pancreatic (alcohol abuse, alters secretions leads to blocked ducts), haemochromatosis (genetic, excess iron deposited), pancreatic trauma, CF, neoplasia,

334
Q

Secondary diabetes to endocrine causes

A

Acromegaly, Cushing’s syndrome, pheochromocytoma
Due to insulin resistance

335
Q

Secondary diabetes to acromegaly

A

insulin resistance due to excess GH simulating gluconeogenesis and lipolysis, causing hyperglycemia and elevated free fatty acid levels

336
Q

Secondary diabetes to Cushing’s syndrome

A

Excess glucocorticoid leads to reduced glucose uptake and increased gluconeogenesis so increase increased insulin resistance

337
Q

Secondary diabetes to Pheochromocytoma

A

Catecholamines excess leads to increase gluconeogenesis and decrease glucose uptake leading to insulin resistance

338
Q

Secondary to drug induced diabetes

A

Glucocorticoids- increase insulin resistance
thiazides/ protease inhibitors/ antipsychotic- not fully understood

339
Q

Pharmacological name for cortisol

A

hydrocortisone

340
Q

Cortisol rising to peak times

A

Starts rising at 3 am to peak shortly before waking up

341
Q

Cortisol decline period

A

From wake up to 7pm

342
Q

Cortisol quiescent period

A

7pm-3am

343
Q

Adrenal insufficiency (AI) causes

A

Primary- Addison’s disease
Secondary- hypopituitarism
Tertiary- suppression of HPA (steroids)

344
Q

Addison’s disease

A

Primary adrenal insufficiency- intrinsic diseases that affect the cortex of the adrenal glands, causing impairment in the synthesis and secretion of all steroids

345
Q

Addison’s disease- Causes

A

Adrenal destruction
Autoimmune- most common
Infections, mets, haemorrhagic infection, surgical removal

346
Q

Secondary adrenal insufficiency

A

Occurs when the pituitary gland doesn’t make enough of the hormone ACTH

347
Q

0900 Cortisol and AI- investigations

A

− Cortisol > 450-500 nmol/l AI unlikely
− Cortisol < 100 nmol/l AI likely

348
Q

ACTH and AI- investigations

A

− ACTH > 22 pmol/l primary
− ACTH < 5 pmol/l secondary

349
Q

Renin / Aldo and AI- investigations

A

− Elevated renin in primary

350
Q

Synacthen Test

A

uses synacthen to test how well the adrenal glands make cortisol
− 250ug IV, measure after 0’ & 30’
− > 450-550 nmol/l AI unlikely

351
Q

Management- Adrenal Crisis

A

Bloods- cortisol +ATCH
Hydrocortisone 100mg IV/IM/SC

352
Q

Treatment of Adrenal insufficiency (AI)

A

Glucocorticoid/ Mineralocorticoid/ Androgen Replacement

353
Q

Sick Day Rules- Adrenal insufficiency (AI)

A

Always carry 10 x 10mg tablets hydrocortisone
* If unwell with fever or flu like illness double dose of steroids
* If in doubt double dose of steroids
* If vomiting or increasingly unwell take emergency injection
of hydrocortisone 100mg IM (SC)
* If unable to have injection take hydrocortisone 20mg 6
hourly and repeat if vomit
* Go to emergency room / ring ambulance

354
Q

Most common complication of type 2 diabetes

A

Cardiorenal- CVD and CKD

355
Q

Aims of type 2 DM treatment

A

Manage blood glucose
Reduce risk of CVD, CKD, microvascular complications
Weight reduction- (increased PA, decreases dietary fat)

356
Q

HbA1c

A

average blood glucose levels for the last 2-3 months

357
Q

Diabetic complications that risk increases with mean HbA1c

A

Diabetic retinopathy, nephropathy, Serve non-proliferative/ proliferative DR, neuropathy, microalbuminuria

358
Q

Treatment options for controlling excess blood glucose in type 2 diabetes

A

Sensitise body to insulin- metformin and pioglitazone
Replace insulin- insulin injections/pumps
Secrete more insulin- sulphonylureas, DPP-4 inhibitors, GLP-1 receptor agonist

359
Q

Initial pharmaceutical therapy for Type 2 DM

A

Metformin

360
Q

Incretins

A

They stimulate pancreatic β-cells after meals, to secrete insulin i.e. glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1)

361
Q

Sodium glucose co-transporter 2 inhibitor (SGLT-2i)

A

Current treatments are act as insulin secretagogues or sensitisers
Kidney key role in glucose homeostasis-glucose reabsorption

362
Q

SGLT-2i limitations

A

Higher risk of infection, more common in women and more often mycotic than bacterial

363
Q

Diabetic Complications

A

Diabetic retinopathy, stroke, CVD, Diabetic nephropathy, peripheral vascular disease, DPN (Diabetic peripheral neuropathy)

364
Q

Diabetic Neuropathy

A

uncontrolled high blood sugar damages nerves and interferes with their ability to send signals, leading to diabetic neuropathy

365
Q

Clinical consequences of Diabetic Neuropathy

A

painful neuropathic symptoms, autonomic neuropathy and insensitivity that results in foot ulceration and amputation

366
Q

Diabetic Peripheral Neuropathy (DPN) and CVD

A

alarming association between DPN and cardiovascular disease

367
Q

Does DPN commonly cause pain

A

Painful symptoms are present in about a third, however pain can disabling

368
Q

Does DPN commonly cause significant motor deficits

A

No, Significant motor deficit is not common

369
Q

Treatment of Diabetic Painful neuropathy

A

Good glycaemic control
Medications to manage Neuralgia - ie
Tricyclic antidepressants / SSRIs
Anticonvulsants
Opioids
IV lignocaine
Capsaicin
Transcutaneous nerve stimulation / acupuncture / spinal cord stimulators
Psychological interventions / hypnosis

370
Q

Diabetic Foot Ulceration (DFU)

A

Foot ulceration occurs in 15% of people with DM during their lifetime, Lower limb amputations X 15 in people with DM2

371
Q

Cause of diabetic amputation- common pathway

A

Neuropathy (damage to the nerves that serve the lower limbs and hands)/ vascular disease (affects the larger vessels of the lower limbs) > trauma >ulcer > failure to heal > infection> amputation

372
Q

Will most people with neuropathy be aware if they are having any problems with their feet

A

most people with neuropathy are insensate (due to sensory nerve damage) and will not be aware of a problem
IMPORTANT TO GET PATIENT TO REMOVE SHOE

373
Q

Euvolemia

A

the state or condition of having the normal volume of blood or fluids in the body

374
Q

Satiety

A

The physiological feeling of no hunger

375
Q

Location where most of the appetite regulation in the brain

A

Hypothalamus

376
Q

Graves disease- thyroid function test

A

If thyroid function test shows high T4+T3, but low TSH, what is the likely diagnosis

377
Q

T4/ T3 may be low/normal in mild hypothyroidism positive titre of TPO antibodies in Hashimoto’s

A

Investigation for Hasimoto’s

378
Q

Hyperosmolar hyperglycaemic state

A

Most common in T2DM
Characterised by profound hyperglycaemia, hyperosmolality and volume depletion in the absence of significant ketoacidosis

379
Q

Hyperosmolar hyperglycaemic state cause

A

Often triggered after infection or acute illness (commonly MI, sepsis + stroke)

380
Q

Hyperosmolar hyperglycaemic state- symptoms

A

Dehydration
Acute cognitive impairment
Polyuria, polydipsia, and weight loss
Weakness
Signs of the underlying cause (commonly MI, sepsis + stroke)

381
Q

Hyperosmolar hyperglycaemic state- 1st order investigations

A

bloods- glucose (high), ketones (-ive or low), U+E, venous blood gas, serum osmolality (high)
ECG- for cardiac precipitants

382
Q

Hyperosmolar hyperglycaemic state- treatment

A

Urgent IV fluids (with K+ replacement if needed)
Insulin
Identify/ treat underlying cause
Monitor biochemical markers
Monitor and treat complications

383
Q

Hyperosmolar hyperglycaemic state- complications

A

cerebral oedema and central pontine myelinolysis
fluid overload

384
Q

Subacute thyroiditis (De Quervain’s thyroiditis)

A

inflammation of the thyroid characterised by a triphasic course of transient hyperthyroidism (up to 6 weeks), hypothyroidism (upto 6 months), followed by a return to euthyroidism

385
Q

Subacute thyroiditis (De Quervain’s thyroiditis)- aetiology

A

Presumed to be viral or autoimmune

386
Q

Subacute thyroiditis (De Quervain’s thyroiditis)-

A

Hyperthyroid- supportive (NSAIDs, if unresponsive corticosteroids)
Hypothyroid- generally don’t require thyroid replacement therapy
Most return to normal thyroid function (90%) but some need long term levothyroxine therapy

387
Q

Thyroid storm

A

happens when your thyroid gland releases a large amount of thyroid hormone in a short amount of time
Medical emergency

388
Q

Thyroid storm causes

A

typically develops in untreated or partially treated hyperthyroidism conditions (ie graves’ disease)
After radioactive iodine therapy because of release of stores of thyroid hormone

389
Q

Thyroid storm presentation

A

volume depletion, congestive heart failure, confusion, nausea and vomiting, and extreme agitation

390
Q

Thyroid storm- treatment

A

high-dose antithyroid drugs, corticosteroids, beta-blockers, iodine solution with supportive care

391
Q

Thyroid- storm investigations

A

Elevated T3, T4
Supressed TSH
Shouldn’t wait before treatment

392
Q

Thyroid cancer types

A

Papillary (60%)- younger pts
Follicular (<25%)- middle age
Medullary (5%)- may produce calcitonin
Lymphoma (5%)

393
Q

Thyroid cancer- common treatment

A

Total thyroidectomy
Iodine ablation
Node clearance

394
Q

Thyroid cancer symptoms

A

Growing lump on thyroid
Hoarse voice
Sore throat
Difficult swallowing or breathing
Pain in front of neck (pressing)

395
Q

Carcinoid tumour

A

a rare cancer of the neuroendocrine system
Typically found on bowels or appendix

396
Q

Carcinoid syndrome

A

collection of symptoms of carcinoid tumour – usually one that has spread to the liver – releases hormones such as serotonin into the bloodstream

397
Q

Carcinoid syndrome- signs and symptoms

A

Bronchoconstriction, paroxysmal flushing (esp in upper body), diarrhoea, congestive cardiac failure

398
Q

Carcinoid syndrome- diagnosis

A

elevated levels of urinary 5-hydroxyindoleacetic acid (waste product that comes from the breakdown of serotonin by the liver)

399
Q

Carcinoid syndrome- treatment

A

Surgery resection (radio+/radiotherapy if surgery not effective)
Management of symptoms

400
Q

Serotonin syndrome

A

excess serotonin in the CNS, resulting from the therapeutic use or overdose of serotonergic drugs

401
Q

Serotonin syndrome- triad of clinical features

A

neuromuscular excitation, autonomic effects, and altered mental status

402
Q

Serotonin syndrome- treatment

A

cessation of offending medication(s) or dose reduction- if mild/ moderate
emergency supportive care if severe

403
Q

Primary aldosteronism (Conn’s syndrome)

A

Aldosterone production exceeds the body’s requirements and is relatively autonomous with regard to RAAS
Most common specifically treatable/ curable form of HTN

404
Q

Primary aldosteronism (Conn’s syndrome)- key diagnostic factors

A

HTN
RFs- family history of primary aldosteronism, of early onset of hypertension and/or stroke

405
Q

Primary aldosteronism (Conn’s syndrome)- 1st order investigation

A

Aldosterone/renin ratio- most reliable screening tool- elevated aldosterone: renin

406
Q

Primary aldosteronism (Conn’s syndrome)- diagnostic test

A

Fludrocortisone suppression test- most reliable
Saline infusion testing + Oral salt loading are alternatives

407
Q

Primary aldosteronism (Conn’s syndrome)- treatment

A

Surgery- (unilateral) laparoscopic adrenalectomy
Aldosterone antagonists

408
Q
A
409
Q

Hyperkalaemia

A

too much K+ in blood
Serum potassium value >6.0 mmol/L

410
Q

Hypokalaemia

A

too little K+ in blood
serum potassium level <3.5 mmol/L

411
Q

Hyperkalaemia- common causes

A

-High intake of potassium in the setting of decreased renal excretion
-Extracellular redistribution of potassium from intracellular locations

412
Q

Hyperkalaemia- acute manifestations

A

muscle weakness
ECG changes (life treating arrhythmia)

413
Q

Hyperkalaemia- ECG changes

A

Peaked T waves and bradycardia
P wave flattening
PR prolongation
Wide QRS complex

414
Q

Hyperkalaemia- ECG changes- pathophysiology

A

Increased extracellular potassium reduces myocardial excitability, with depression of both pace making and conducting tissues.

415
Q

Hyperkalaemia- common differentials

A

Chronic kidney disease
Diabetic ketoacidosis/hyperosmolar hyperglycaemic state
Potassium supplementation with underlying renal dysfunction
Drug induced

416
Q

Hypokalaemia- common causes

A

urinary or GI losses

417
Q

Hypokalaemia- acute manifestations

A

muscle weakness and ECG changes

418
Q

Hypokalaemia- prolonged manifestations

A

rhabdomyolysis (destruction of striated muscle cells), renal abnormalities, and cardiac arrhythmias

419
Q

Hypokalaemia- ECG changes

A

T wave inversion
St depression
Prominent U waves

420
Q

Hypokalaemia- ECG- Push-pull effect

A

Hypokalaemia creates the illusion that the T wave is “pushed down”, with resultant T-wave flattening/inversion, ST depression, and prominent U waves

421
Q

Hyperkalaemia- ECG- Push-pull effect

A

In hyperkalaemia, the T wave is “pulled upwards”, creating tall “tented” T waves, and stretching the remainder of the ECG to cause P wave flattening, PR prolongation, and QRS widening

422
Q

Hypokalaemia- common differentials

A

Vomiting, severe diarrhoea, eating disorders, alcoholism, drug induced, primary aldosteronism, DKA, Hyperosmolar hyperglycaemic state, Exercising in a hot climate
Stress response in critical illness

423
Q

Parathyroid hormone

A

Normally secreted in response to low Ca2+ from parathyroid glands, controlled by a -ve feedback loop via Ca2+ levels

424
Q

Parathyroid hormone- action

A

-Increase osteoclast activity producing PO(4)3- and Ca2+
-Increase Ca2+ and decrease PO(4)3- reabsorption in the kidneys
-Increased active 1,25 dihydroxy-vitamin D3

425
Q

Parathyroid hormone- overall action

A

Increased Ca2+
Decrease PO(4)3-

426
Q

Hyperparathyroidism

A

Too much parathyroid hormone
3 types- primary, secondary, tertiary

427
Q

Primary hyperparathyroidism

A

Parathyroid gland produces too much Parathyroid hormone

428
Q

Primary hyperparathyroidism- causes

A

-80% solitary adenoma
-20% hyperplasia
- <0.5% parathyroid cancer

429
Q

Primary hyperparathyroidism- presentation

A

Often asymptomatic
Signs relate to- hypercalcaemia, increased bone resorption or HTN

430
Q

Hypercalcaemia- signs

A

Weak, tired, depressed, thirsty, dehydrated-but-polyuric
Also renal stones, abo pain, pancreatitis, ulcers

431
Q

Increased bone resorption- signs

A

Bone pain, fractures, osteopenia, osteoporosis

432
Q

Primary hyperparathyroidism- diagnostic test

A

Increased serum Ca2+ and inappropriate elevation of PTH

433
Q

Primary hyperparathyroidism- Indications for surgery

A

Symptomatic
Or asymptomatic with <50 yrs, vry serum Ca2+, low eGFR, osteoporosis, lumbar spine, total hip, femoral neck, or distal third of radius, and/or vertebral fracture

433
Q

Primary hyperparathyroidism- definitive treatment

A

Parathyroidectomy

434
Q

Primary hyperparathyroidism- treatment for asymptomatic with no surgical indications

A

Monitoring- serum Ca2+, BMD T-score, lumbar spine, fracture scan
Vitamin D supplementation for those deficient

435
Q

Secondary hyperparathyroidism

A

elevation of PTH secondary to hypocalcaemia

436
Q

Secondary hyperparathyroidism- causes

A

Vit D deficiency, chronic renal failure

437
Q

Secondary hyperparathyroidism and chronic renal failure

A

Defect in the activation of vitamin D in the kidneys due to chronic kidney disease leads to hypocalcaemia, resulting in compensatory PTH production causing secondary hyperparathyroidism

438
Q

Secondary hyperparathyroidism- diagnostic test

A

Low serum Ca+, Elevated (appropriately) PTH

439
Q

Secondary hyperparathyroidism- treatment

A

Correct underlying cause
Phosphate binders, Vit D, cinacalcet if needed

440
Q

Chvostek’s sign

A

Tapping on the face just anterior to the ear and seeing a twitching of muscles around the mouth. Seen in most hypocalcaemic states. Demonstrates neuromuscular excitability.

441
Q

Trousseau’s sign

A

Inflating blood-pressure cuff above diastolic for about 3 minutes causes muscular flexion of the wrist, hyperextension of the fingers, and flexion of the thumb. Seen in most hypocalcaemic states. Demonstrates neuromuscular excitability.

442
Q

What do Chvostek’s and Trousseau’s sign represent

A

Hypocalcaemia Demonstrates neuromuscular excitability.

443
Q

Tertiary hyperparathyroidism

A

High Ca2+ and very high PTH (inappropriately)
Occurs in chronic renal failure

444
Q

Tertiary hyperparathyroidism- pathophysiology

A

Occurs after prolong secondary hyperparathyroidism, causing gland to act autonomously having under gone hyperplasic or adenomatous change
This causes increased Ca2+ from very increased PTH secretion by feedback control

445
Q
A

Phase 2a Lecture Notes (14 decks)

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