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3rd BDS IHD > Endocrine > Flashcards

Endocrine Flashcards

1
Q

what is the relationship between hypothalamus, pituitary and adrenal gland

A

hypothalamus releases releasing hormones to pituitary in brain
pituitary releases secreting hormones to adrenal
adrenal gland feeds back to hypothalamus

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2
Q

what things can go wrong with glands (3)

A

overproduction
underproduction
benign/malignancy

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3
Q

where do we find adrenal glands

A

1 on the superior aspect of each kidney

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4
Q

what is the shape and structure of an adrenal gland

A

triangular/pyramidal in shape
Composed of cortex and medulla.
Cortex (outer part) composed of three layers; zona glomeruloa (produces aldosternone), zona fasciculata (produce cortisol), zona reticularis (produce androgenic steroids).
Medulla (inner part of gland) produces stress hormones (adrenaline and noradrenaline).

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5
Q

what is the cortex of the adrenal gland split into and what do they produce

A

Cortex (outer part) composed of three layers; zona glomeruloa (produces aldosternone), zona fasciculata (produce cortisol), zona reticularis (produce androgenic steroids).

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6
Q

what does the medulla of the adrenal gland produce

A

produces stress hormones (adrenaline and noradrenaline).

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7
Q

how can we detect adrenal problems

A

24 hour cortisol urine test
Serum ACTH levels
Diurnal pattern of serum cortisol levels
Dexamathasone suppression test

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8
Q

what are the 3 main pathway causes of adrenal problems

A

Secondary: disease of pituitary or hypothalamus
Primary: adrenal disease: Developmental, haemorrhagic necrosis, autoimmunity, destruction by TB or tumour
Iatrogenic: Suppression due to steroid therapy

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9
Q

if the adrenal gland is yellow and cheese like in the middle, what is the likely cause

A

tuberculosis

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10
Q

what does Waterhouse-Friderichsen syndrome affect and how does it resent

A

causes haemorrhage of the adrenal gland cortex
adrenal glands turn black with blood clot

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11
Q

what are some effects of adrenal insufficiency

A

Skin pigmentation
Hypotension
Muscle weakness
Hypoglycaemia
Hyponatraemia
Hyperkalaemia
Renal dysfunction

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12
Q

what are some causes of adrenal overactivity

A

Cushing’s syndrome - adrenal tumours, iatrogenic
Cushing’s disease – pituitary microadenomas
Conn’s syndrome - excessive aldosterone

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13
Q

compare cushing’s syndrome and cushings disease

A

Cushing’s syndrome - adrenal tumours, iatrogenic
Cushing’s disease – pituitary microadenomas

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14
Q

what does Cushing’s syndrome cause

A

Obesity
Hypertension
Osteoporosis
Hyperglycaemia
Myopathy
Skin atrophy
Polycythaemia
Susceptibility to infection

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15
Q

what is Paroxysmal hypertension and what is this a key sign of

A

rapid increase in blood pressure that slightly decreases over time
sign of Phaeochromocytoma

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16
Q

what is Phaeochromocytoma and what is its key symptom

A

Tumour adrenal medulla forming a catecholamine producing tumour
Paroxysmal hypertension

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17
Q

how do we decide the behaviour of pheochromocytoma

A

PASS: pheochromocytoma of adrenal gland scoring system.
Could be malignant or benign. Metastasis is indicator of malignancy.

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18
Q

what is the pathway of thyroid gland secretions

A

hypothalamus secretes thyroid releasing hormone TRH
pituitary released thyroid stimulating hormone TSH
thyroid releases T3 and T4 - inhibit hypothalamus and pituitary

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19
Q

how might we diagnose thyroid problems

A

Serum T3, T4, TSH, calcitonin

Ultrasound

Radioactive iodine uptake studies

FNA cytology - fine needle aspiration

Core biopsy

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20
Q

why is cytology good for thyroid diagnosis and why might it be disadvantageous

A

Safe- Reduces need to excise benign lesions
Thy 1-5 categories
Can establish diagnosis of some types carcinoma: papillary, medullary, anaplastic
Can’t distinguish between benign and malignant follicular lesions

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21
Q

which type of thyroid cancer can cytology not differentiate between malignant and benign

A

follicular

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22
Q

what might cause hypothyroidism

A

Iodine deficiency
Developmental
Autoimmune
Radiotherapy, radioiodine therapy
Drugs

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23
Q

what might cause hyperthyroidism

A

Autoimmune
Toxic adenomas
masses

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24
Q

what is goitre

A

swollen thyroid gland = large swollen neck

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25
Q

name the 2 most common autoimmune thyroid disorders

A

Hashimoto thyroiditis

Graves disease

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26
Q

what is hashimoto thyroiditis and who is likely to get this and what does it present as

A

Middle aged, women
Auto-antibodies against Thyroglobulin and Thyroid peroxidase
Lymphocyte mediated destruction of thyroid follicles

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27
Q

how would hashimoto thyroiditis present clinically and histologically

A

Initial hyperthyroidism followed by hypothyroidism
Painless enlarged thyroid
histologically Lymphocyte mediated destruction of thyroid follicles

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28
Q

how do we treat hashimoto thyroiditis

A

life long thyroxine

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29
Q

what 2 risks are there from having hashimoto thyroiditis

A

Risk of developing other autoimmune disease

Low Risk for thyroid malignancy

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30
Q

what is Graves disease

A

most common cause of hyperthyroidism
Production of Thyroid stimulating immunoglobulin
Anti-TSH receptor antibodies
Diffuse process histologically affecting all of the lobe and both lobes
can lead to cellulitis

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31
Q

how would a Graves disease blood test present

A

Elevated T3 and T4. Low TSH

Increased uniform radio-iodine uptake

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32
Q

how do we treat graves disease (3)

A

Treated with anti-thyroid medications
radio-iodine ablation
surgery

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33
Q

what is the most common benign neoplasm of the thyroid gland

A

Follicular adenoma
usually solitary encapsulated

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34
Q

what is the most common malignancy in thyroid tissue

A

papillary carcinoma 60-70% of cases
in young adults
lymphatic spread - good prognosis usually

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35
Q

what is the prognosis of papillary carcinoma of the thyroid and why

A

usually good
metastasises via lymph nodes, not blood

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36
Q

how would papillary/follicular carcinomas look histologically

A

optically clear nuclei ‘orphan annies eyes’
overlapping nuclei
overcrowding

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37
Q

if thyroid tissue has clear overcrowded nuclei, what is the likely diagnosis

A

papillary carcinoma

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38
Q

compare follicular and papillary carcinomas of thyroid

A

papillary : 60-70% of carcinomas, young adults, good prognosis, lymph spread
follicular: 20-25%, young-middle age, blood stream, worse prognosis

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39
Q

how might we know if a thyroid cancer is malignant histologically

A

clear nucelli - papillary carcinoma
vascular invasion into the blood vessel
capsular invasion

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40
Q

what is the least common thyroid carcinoma

A

medullary 5-10%
elderly but familar cases earlier in life
lymphatic and blood stream spread
variable prognosis

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41
Q

thyroid cancer has spindle cell morphology, what type of carcinoma is this?

A

medullary

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42
Q

calcitonin histocytochemistry can be used to diagnose what and how would it show and what else would give this stain

A

medullary carcinoma
stain tissues brown
C cell hyperplasia

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43
Q

what type of cell does medullary carcinoma affect

A

C cells

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44
Q

if a thyroid cancer has nests of cells, signs of necrosis and increased mitosis what ttype of carcinoma is this

A

poorly differentiated carcinoma

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45
Q

why is anaplastic carcinoma very low prognosis

A

it has very aggressive local spread

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46
Q

what is anaplastic thyroid carcinoma

A

occurs in elderly with very agressive local spread = very poor prognosis
very varied cells and nuclei

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47
Q

what is the commonest cause of thyroid lymphoma

A

hashimotos thyroiditis

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48
Q

what does insulin do

A

convert glucose to glycogen = reduced glucose blood levels

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49
Q

what does glucagon do

A

convert glycogen to glucose
increase glucose blood concentrations

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50
Q

in the fasting state, where do w get glucose from (2)

A

mainly the liver, sometimes the kidney

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51
Q

what percent of glucose goes to muscle and liver after eating

A

40% goes to the liver
60% goes to muscle

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52
Q

if glucose and glycogen is low in fasting state, what do we use for energy

A

lipids and FFA free fatty acids
beta oxidation
forms ketone bodies as a side product

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53
Q

what part of the pancreas produces glucagon and insulin (3)

A

endocrine section of pancreas
islets of langerhans
beta cells = insulin
alpha cells = glucagon

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54
Q

explain the paracrine hypothesis with glucose homeostasis

A

this explains crosstalk between beta and alpha cells
high insulin levels keep alpha cells inhibited
when insulin drops (due to low glucose), alpha cells are no longer inhibited
therefor produce glucagon

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55
Q

what does glucose pass through to enter a beta cell of the pancreases

A

GLUT2 receptor

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56
Q

explain glucose action on a beta cell (how this leads to insulin release)

A

glucose enters cell via GLUT2 channel
reaction occurs glucose (glucose kinase) –> ATP/ADP
this closes potassium channel = depolarized cell membrane
calcium channels open and calcium enters
Calcium triggers insulin release

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57
Q

explain how insulin acts on a fat/muscle cell

A

insulin attaches to insulin receptor
cascade of reactions activating intracellular GLUT4 vesicles
mobile GLUT4 vesicles integrate to plasma membrane
allows glucose to enter the cell

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58
Q

explain how insulin acts on a fat/muscle cell

A

insulin attaches to insulin receptor
cascade of reactions activating intracellular GLUT4 vesicles
mobile GLUT4 vesicles integrate to plasma membrane
allows glucose to enter the cell

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59
Q

what is the name of the vesicle that insulin acts on

A

intracellular GLUT4 vesicle

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60
Q

give the 3 major affects of insulin

A

supresses hepatic glucose output e.g. gluconeogenesis and glycogenolysis
increase glucose uptake by insulin sensative cells e.g. fat and muscle
supresses lipolysis and muscle breakdown

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61
Q

what is a counterregulatory hormone and give examples

A

hormones that oppose the action of insulin
glucagon
also adrenaline, cortisol, growth hormone

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62
Q

what is the action of counterregulatory hormones (3)

A

opposite of insulin
1. increases hepatic glucose output e.g. gluconeogenesis and glycogenolysis
2. decreases glucose uptake in sensitive cells e.g. fat and muscle
3. stimulate peripheral release of glucose, FFAs and muscle breakdown

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63
Q

what is the risk of a diabetic having high adrenaline

A

adrenaline is a counterregulatory hormone, opposing insulin action

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64
Q

what are symptoms of HYPOglycemia

A

sweating
feeling tired
dizziness
feeling hungry
tingling lips
feeling shaky or trembling
a fast or pounding heartbeat (palpitations)
becoming easily irritated, tearful, anxious or moody
turning pale

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65
Q

what are symptoms of hyperglycaemia

A

feeling very thirsty
peeing a lot
feeling weak or tired
blurred vision
losing weight

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66
Q

what is diabetes mellitus

A

disorder of carbohydrate metabolism and homeostasis leading to hyperglycaemia

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67
Q

what can acute hyperglycaemia cause (2)

A

diabetic ketoacidosis DKA
hyperosmolar hyperglycaemic state = coma

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68
Q

what can chronic hyperglycaemia cause

A

tissue complications with vessels e.g. blood vessels in heart, brain, periphery, legs
limbs = amputation
brain = stroke
heart = heart failure
mouth = bleeding and periodontitis

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69
Q

what are the 3 types of problems that come with diabetes

A

acute hyperglycaemia = diabetic ketoacidosis (DKA) and hyperosmolar coma (Hyperosmolar Hyperglycaemic State )
chronic hyperglycaemia = tissue complications = stroke, leg arteries = amputation
medication related hypoglycaemia

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70
Q

what oral symptoms of diabetes are there (4)

A

slow wound healing in the mouth
halitosis = ketone bodies
increased periodontitis and BOP
oral candidiasis = reduced fungal response

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71
Q

a patient has oral candidiasis and slow healing wounds in the mouth. What could they have

A

undiagnosed diabetes

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72
Q

what types of diabetes are there (5)

A

type 1
type 2 (including gestational)
MODY - Maturity onset diabetes of youth (MODY), also called monogenic diabetes
pancreatic diabetes
“Endocrine Diabetes” (Acromegaly/Cushings)

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73
Q

what is pancreatic diabetes

A

where there is uncontrolled glucose homeostasis due to an insult to the pancreas
possibly trauma or surgery or cancer altering the function of the pancreases

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74
Q

what is MODY

A

Maturity onset diabetes of youth (MODY), also called monogenic diabetes
diabetes caused by a genetic factor

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75
Q

why does uncontrolled diabetes lead to thirst

A

the kidney usually reabsorbs all glucose back into the blood
can only absorb 11mol/L
over this amount, glucose stays in the collecting duct
glucose acts as an osmotic agent pulling more fluid into the collecting duct, increasing volume of urine
body looses more fluid, therefor pt gets more thirsty

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76
Q

how much glucose can a healthy kidney reabsorb

A

11mol/L

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77
Q

how long do red blood cells stay in the body and where do they get destroyed after this time

A

remain in the blood stream for 120 days
then get decommissioned in the spleen

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78
Q

what is the HbA1c level and why is this significant

A

amount of glycated haemoglobin
above 48mmol/mol or 6.5% = diabetic

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79
Q

why do we have to be careful using HbA1c levels for diabetes detection (2)

A

any problem that alters RBC presence or destruction e.g. splenomegaly or acute blood loss = false negative
iron deficiency anaemia can make RBC last longer and give false positives

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80
Q

how does iron deficient anaemia affect HbA1c levels

A

this leads to RBC lasting longer in the blood stream
gives higher levels of HbA1c = false positive diabetes

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81
Q

what diagnostic values are there for positive diabetes

A

random blood glucose levels > 11mmol/L
fasting plasma glucose levels > 7mmol/L repeated 2 times
HbA1c levels > 48mmol/mol 6.5%

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82
Q

what is the type I diabetes

A

autoimmune disease where a cross reaction leads to antibodies that attack beta cells of the islets of Langerhans possibly due to a virus
no beta cells
no insulin production

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83
Q

why does type I diabetes lead to hyperglycaemia (3)

A

no insulin therefor:
-glucagon levels remain high
-no glucose uptake in insulin sensitive cells
-hepatic breakdown of glycogen and fats

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84
Q

what would be the cause of death in a type I diabetic uncontrolled state

A

diabetic ketoacidosis

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85
Q

explain why diabetic ketoacidosis is dangerous and how it comes about

A

occurs as body needs fuel but cannot use glucose as it is all in the vessels
uses fat beta oxidation for fuel
side product is ketones
ketones as slightly acidic and builds up in the blood = poison
causes vomiting, passing a lot of water, hyperventilating to remove acidic CO2
leads to dehydration and kidney failure

86
Q

what is the bodies reaction to diabetic ketoacidosis (4)

A

vomiting due to blood poisoning
polyuria and polydypsia
hyperventilation to remove acidic CO2
loose weight as we are loosing glucose (urine) and fat (beta oxidation)

87
Q

what two factors lead to impaired insulin tolerance in type II diabetes

A

impaired insulin secretion (genetic)
acquired insulin resistance (environmental)

88
Q

why does insulin resistance occur

A

increased weight = increased fat = larger cells and change in morphology of the cells and receptors = insulin resistance

89
Q

why might a type II diabetic be on insulin injections

A

after about 10 years body declines in insulin sensitivity
may be complete insulin resistant

90
Q

do macrovascular or microvascular problems come first in pre-diabetes

A

macro come first

91
Q

how many grams of sugar do we give to test the pancreas for diabetes

A

75 grams

92
Q

what is treatment for hypoglycaemia

A
93
Q

how do we treat type II diabetes

A

exercise and weight loss
controlled diet
control blood pressure and other symptoms
possibly insulin shots if progressive type II diabetes = insulin resistance

94
Q

what is gliclazide mainly used for

A

treatment of type 2 diabetes
type of sulphnylureas that keeps potassium ion channel shut = release of insulin

95
Q

what must we ensure a patient does before a dental procedure if they are on gliclazide and why

A

eats breakfast before
glyclazide is a sulphonylureas and increases insluin
if not eationg = hypoglycaemic attack

96
Q

what are Sulphonylureas and give the main type of this drug

A

drug used for type 2 diabetes top increase insulin secretion
gliclazide

97
Q

how do sulphonylureases work

A

close K+ channels on beta cells in pancreas
causes depolaization by Ca2+ and insulin release
type 2 diabetes

98
Q

what 2 risks come with medication for type II diabetes

A

weight gain
hypoglycaemia

99
Q

what are DZTs used for

A

type II diabetes

100
Q

what 6 types of medication might a type II diabetic be on

A

first line
Metformin
second line
DZTs
GLP-1 analogues
DPP-Iv inhibitors (stop break down of GLP-1)
SGLT2
replacing sulphonyureases e.g. gliclazide

101
Q

what are the affects of GLP-1 analogues

A

stimulate insulin secretion
reduce apatite
slow gastric emptying
improve insulin sensitivity

102
Q

where is GLP-1 secreted and what is its function and how do we use this theraputically

A

L cells in the duodenum
causes slower gastric emptying, reduces apatite, increases insulin sensitivity and production
to make us feel full and not eat any more
GLP-1 analogue drugs used in type II diabetes

103
Q

how do DPP-IV inhibitors work (4)

A

DPP-IV is an enzyme that breaks down GLP-1
GLP-1 is secreted by L cells of the duodenum
GLP-1 causes insulin sensitivity, decreased gastric emptying, decreased hunger, insulin release, glucagon inhibition
type II diabetes

104
Q

what type of drug are vidagliptin and sagliptin

A

DPP-IV inhibitors
suffix ‘gliptin’
prevent breakdown of GLP-1 for type II diabetes

105
Q

what is gliptin the suffix for

A

medications of the class DPP-Iv inhibitors for type II diabetes
prevent breakdown of GLP-1

106
Q

what medication other than insulin can be used in type I and II diabetes

A

SGLT2
prevent reabsorption of glucose in the kidney

107
Q

what is the main side effect of SGLT-2

A

genital thrush

108
Q

how do SGLT2 work

A

prevent reabosprtion of glucose in the kidney

109
Q

what is astrflozin, glutaflozin and canagliflozin

A

SGLT2 drugs
prevent reabsorption of glucose in the kidney

110
Q

what is the suffix ‘ flozin ‘ for

A

SGLT2 diabetes medication
prevent reabsoprtion of glucose in the kidney

111
Q

what is the first line drug for type II diabetes

A

metformin

112
Q

how does metformin work

A

reduce production of glucose by the liver
decrease absorption of glucose by the gastrointestinal tract
and increase target cell insulin sensitivity

113
Q

other than fingerpick monitoring, how else can we monitor blood glucose

A

continuous glucose monitoring device e.g. libre

114
Q

what is a limitation of continuous blood glucose monitoring devices

A

they test the interstitial fluid glucose levels which might not represent blood glucose levels in real time

115
Q

how do we treat hypoglycaemic attack

A

20g of rapidly acting carbohydrate e.g. glucose syrup
slow release carbohydrate afterwards to manage

116
Q

what hormones does thyroid gland produce with their roles

A

thyroxine T4
T3 tri-iodotryonine
both control basal metabolic rate
calcitonin - regulates calcium levels in the blood

117
Q

what is unique about the thyroid gland

A

stores high amounts of inactive hormone in extracellular follicles
also largest endocrine gland in body

118
Q

what happens if a healthy individual goes into hypoglycaemia and how does this change in diabetes

A

glucagon, cortisol and adrenaline (counterregulatory hormones) released
in diabetes, if the pt has many hypo attacks, their resistance to it dampens and they may not have the same respsonse
meaning when in hypo, they may not show common adrenaline symptoms e.g. sweating
so hypo may be more difficult to spot

119
Q

compare primary and secondary hypothyroidism

A

primary = thyroid underproducing T4 and T3
secondary = pituitary or another factor leading to less TSH and therefor less T3 and T4

120
Q

what aspects of the type of hypothyroidism affect goitre

A

T3 and T4 dont make a difference
if TSH is increased, this is driving the thyroid to produce more = enlarged thyroid gland = goitre

121
Q

what type of hypothyroidism doesn’t lead to goitre

A

secondary hypothyroidism as no TSH to drive hyperplasia

122
Q

what are some major symptoms of hypothyroidism

A

tiredness and increased sleep
mennorhagia
macroglossia
cold intolerance
central swelling (large stomach and breast)
dry skin
weight gain

123
Q

what are some facial features of hypothyroidism

A

macroglossia
periorbital oedema
delayed eruption
enamel hypoplasia
thick lips
facial puffiness

124
Q

causes of primary hypothyroidism (4)

A

autoimmunity - hoshimotos thyroiditis
iodine deficiency
post radioactive iodine for hyperthyroidism
thyridectomy

125
Q

causes of secondary hypothyroidism (3)

A

pituitary tumours
pituitary granulomas
empty sella

126
Q

give indications for thyroid screening

A

past radiation
symptoms
congenital hypothyroidism

127
Q

what is the main cause for hyperthryoidism

A

autoimmune disease
e.g. graves disease

128
Q

what are common symptoms of hyperthyroidism

A

heat intolerance
palpitations
anxiety and irritability
weight loss
loose bowels
tachycardia
warm moist skin

129
Q

what might lead us to try and diagnose graves disease

A

hyperthyroidism signs and symptoms
history of other autoimmune disease
diffuse goitre
bulging eye signs oedema
red shins

130
Q

what are the eye signs of graves disease

A

eye lids retracted
can see the sclera above the iris
dryness of eyes
bulging eye

131
Q

how do we treat hyperthyroidism

A

anti-thyroid medication for 12 months
stop treatment, 50% will never get hyperthyroidism again, 50% will
if they do, surgery or raidoactive iodine (sometimes straight to this)

132
Q

what are some dental signs of hyperthyroidism

A

accelerated eruption
mx/mn osteoperosis
increased suseptability to caries and periodontal disease

133
Q

what are some dental considerations for hyperthyroidism

A

Increased susceptibility to caries
Periodontal disease
Increased sensitivity to epinephrine which may result in arrhythmias or palpitations
Surgery, oral infection and stress may precipitate thyroid crises

134
Q

if we see a thyroid nodule what do we do

A

ask about onset
history of nodule
record size
refer for ultrasound

135
Q

what special test would we do for a thyroid nodule

A

ultrasound
thyroid level tests
if NOT hyperthyroid, give FNA

136
Q

why would we not FNA a patient who is hyperthyroid

A

push them into hyperthyroid crisis

137
Q

why would we FNA a thyroid nodule

A

if they are not hyperthyroid and they have an abnormal ultrasound
Fine needle aspiration gives us a histological diagnosis to see if the nodule is benign or malignant

138
Q

what does the anterior pituitary gland produce with their peripheral actions (4)

A

LH and FSH –> oestrogen and androgen
GH –> IGF-1
TSH –> T3 and T4
ACTH –> cortisol

139
Q

what does the posterior pituitary gland gland

A

produced in hypothalamus, stored in pituitary
Vasopressin ADH - water absorption
oxytocin- uterine contractions and milk

140
Q

what (types) symptoms of pituitary dysfunction (3)

A

hormone excess - too much cortisol = cushings or acromegaly
mass excess = headache, double vision, loss of peripheral vision
hormone deficency = lack of growth, lack of cortisol, hypothyroid

141
Q

what special investigation do we do if we suspect pituitary problems

A

MRI

142
Q

what hormonal symptoms might indicate pituitary problems

A

low sperm count/infertility/loss of erections/loss of period
hypothyroidism
short growth and lack of energy
adrenal failure
diabetes incipidus

143
Q

what is ADH used for

A

water reabsorption in the kidneys

144
Q

what is diabetes insipidus and its cause

A

lack of ADH
lack of reabsorption in the kidneys
polyuria and polydipsia

145
Q

what is sheehans syndrome

A

post pregnancy if mother lost a lot of blood
leads to infarct in pituitary
hypopituitary

146
Q

what causes hypopituitary

A

damage
radiotherapy
infarction
trauma
tumour
infection e.g. TB and syphilis
Sheehan syndrome (post pregnancy)

147
Q

after head injury, the patient starts urinating a lot and isnt recovering
what might be the cause

A

pituitary trauma
lack of ADH and cortisol

148
Q

how do we test for acromegaly

A

IGF levels and then MRI of pituitary

149
Q

after surgery how can we treat acromegaly

A

radiotherapy and medications such as somatostatin (acts against growth hormone)

150
Q

pt on somatostatin, what does this treat

A

NOT HIGH BP
inhibits IGF-1 treats acromegaly

151
Q

pt has widening teeth spaces and sleep apnoea, what could be the cause

A

acromegaly

152
Q

what happens to cortisol throughout the day and why is this important to know

A

highest peak at 1 hour after waking
gradually go down to sleep
low overnight
take into account when testing cortisol levels

153
Q

what is cushing’s syndrome

A

where adrenal gland produces too much cortisol

154
Q

what are some causes of cushings syndrome (4)

A

pituitary tumour 70-80%
adrenal tumour 10-20%
eptopic tumour e.g. lunch 10%
MOST COMMON iatrogenic = steroids from medications

155
Q

what are symptoms of cushings syndrome

A

weight gain
moon face - bull neck
bruising
‘buffalo hump’
acne
stretch marks
diabetes

156
Q

how do we test for Cushing’s syndrome

A

give pt a steroid the night before
healthy pt = steroid levels go down
cushings = pt keeps producing steroid

157
Q

if we get a positive steroid supression test, what is the next step

A

MRI of pituitary or CT of adrenal glands

158
Q

pt has central obesity and purple strecth marks. what is the cause of this

A

cushings syndrome

159
Q

what is the name for primary adrenal insufficency

A

addisons disease

160
Q

what type of disease is addisons disease

A

primary adrenal insufficiency

161
Q

why do patients with addisons disease get pigmentation

A

Addison’s disease is adrenal insufficiency
pituitary gland produces Melanocyte stimulating hormone MSH
if cortisol is reduced, the pituitary gland is not inhibited so produces more ACTH and more melanocyte stimulating hormone MSH
leads to dark pigmentation of the skin

162
Q

pt has dark pigmentations in their mouth, what is this

A

addisons disease
primary adrenal insufficiency
lack of cortisol = lack of pituitary inhibition = more release ofLMSH melanocyte stimulating hormone

163
Q

what is secondary adrenal insufficiency

A

where pituitary gland doesnt produce any ACTH so reduced cortisol

164
Q

what are primary causes of primary adrenal insufficency

A

autoimmune
tubercerlosis
fungal infection
congenital adrenal hypoplasia

165
Q

what are the causes of secondary adrenal insufficency

A

medication of steroids!!! if pt on steroids for long time have reduced reliancy on adrenal gland so if they go into a stressful situation or infection, they need more steroids to prevent adrenal crisis
tumour in pituitary or hypothalamus

166
Q

a patient is on predisolone for 10 years and has an abscess. how do we treat, non surgically?

A

antibiotics e.g. metronidazole
AND STEROIDS as infection means stress and secondary adrenal insiufficency
if no added steroids, patient will go into adrenal crisis

167
Q

what is the death rate of adrenal crisis

A

6-8%

168
Q

what percent of the population is on steroids and have adrenal insufficency

A

3% on steroids
50% of them have adrenal insufficency

169
Q

what are signs of adrenal insufficency

A

weakness
loss of weight
vomiting
hypotension
salt craving
hypoglycaemic episodes
IF PRIMARY = skin pigmentation

170
Q

how do we investigate adrenal insufficiency

A

inject with ACTH
test for cortisol spike

171
Q

if a pt is on steroids, what steroid precautions must we take for a minor procedure

A

if high enough e.g. >7mg prednisolone
double dose one hour before surgery
double dose for 24 hours after surgery

172
Q

if a pt is on steroids, what steroid precautions must we take for a major procedure (GA)

A

100mg IM of hydrocortisone before procedure
double oral dose for 24 hours after

173
Q

what 4 main endocrine problems must we understand and treat before dental surgery and why

A

adrenal suppression : double oral dose or give 100mg hydrocortisone IM
hyperthyroidism: must slow down thyroid before or = thyroid crisis
Cushing’s syndrome: high steroid = avoid infections and pathological fracture so control
Phaechromocytoma: adrenal gland too much adrenaline, if not treated this can cause excess adrenaline and cardiac arrest

174
Q

what are endocrine causes of hypertension (4)

A

primary aldosteronism = renal gland = too much aldosterone
pheochromocytoma = too much adrenaline
acromegaly = too much GH
cushings syndrome = secreting excess steroids
hyperthyroidism (not strong relationship)

175
Q

what is calcium important for (4)

A

coagulation factors
nervous function
skeletal mineralization
membrane polarization e.g. muscle contraction, release of insulin

176
Q

what is the function of PTH (1) and how does it act (3)

A

to increase calcium in the blood
increase bone resorption
increase calcium re-absoprtion and reduces phosphate re-absorption in kidney
increase calcium absorption in intestine (by activating vitamin D)

177
Q

what are some causes of hypocalcaemia (4)

A

post surgery/radiotherapy
inherited autosomal dominant hypocalcaemia
syndromes e.g. Di George
chronic renal failure (kidney needed for vitamin D activation)
acute pancreatisis
magnesium deficiency - mg needed to stimulate pth release
pseudohypothyroidism

178
Q

why does renal failure cause hypocalcaemia

A

kidney is site of vitamin D activation
Vitamin D upregulates calcium absoprtion

179
Q

what are the affects of low Mg levels in the blood

A

hypocalcaemia
need magnesium to stimulate PTH release
low PTA = low calcium

180
Q

what is pseudoparathyroidism

A

where we produce PTH however the tissues that accept PTH are less sensative to PTH = low calcium

181
Q

if someone has multiple blood transfusions, what might they acquire

A

hypocalcaemia

182
Q

what are the symptoms and signs of hypocalcaemia

A

muscle spasms in larynx, hands and legs
seizures
dental hypoplasia
long QT interval on ECG

183
Q

someone who is chronically hypocalcaemia has an ECG. what will it look like

A

long QT interval
arrythmic

184
Q

what are 2 examination tests to test hypocalcaemia

A

chvostek’s sign = tap facial nerve = spasm of facial muscle
Trouseau’s sign = inflate BP to 20mmHg above normal for 5 minutes, hand goes into spasm

185
Q

explain chvostek’s sign

A

a test for hypocalcaemia
tap on the facial nerve near the ear
facial spasm of muscles

186
Q

explain Trouseau’s sign

A

test for hypocalcaemia
inflate BP by 20mmHg above normal systolic pressure for 5 minutes
hand goes into spasm

187
Q

what are some things to look out for for hypocalcaemia

A

history of neck surgery/scar
other autoimmune conditions
family history of hypocalcaemia
anti-epileptics
growth failure/hearing loss

188
Q

what are the two main causes of hypocalcaemia

A

low magnesium (needed for PTH stimulation)
low vitamin D (activated in kidney to increase calcium absorption)

189
Q

how do we treat hypocalcaemia (4)

A

if low vitamin D - give unactivated vitamin D
if low Mg = give Mg
calcium supplements
if surgery on thyroid/parathyroid then give activated vitamin D as PT is needed for activation

190
Q

at what point does a hypocalcaemic patient become ‘severe’ and need IV calcium

A

<1.9mmol/mol

191
Q

what are the main 2 causes of hypercalcaemia

A

primary hyperparathyroidism
myeloma/ bone mets/tumour in parathyroid gland
(drugs e.g. calcium drugs)

192
Q

what are some causes of hypercalcaemia

A

primary hyperparathyroidism
myeloma/ bone mets/tumour in parathyroid gland
(drugs e.g. calcium drugs)
phaechromocytoma
immobilisation
lots of milk/alkali
thiazides
adrenal insufficiency

193
Q

what are symptoms of hypercalcaemia

A

thirst
polyuria
nausea
constipation
confusion

194
Q

what are symptoms of hypercalcaemia

A

thirst
polyuria
nausea
constipation
confusion

195
Q

what are some consequences of hypercalcaemia

A

gastric ulcer
weak bone density/fractures
ECG abnormalatis short QT interval
renal stones
pancreatitis

196
Q

what 4 medications must we look for in hypercalcaemia

A

thiazides (high BP)
lithium for mental health
calcium supplements
vitamin D

197
Q

what is tertiary hyperparathyroidism and what causes it

A

where we get enlarged PT gland = hypercalcaemia
chronic kidney failure = low vit D (or just vit D deficency) = hypocalcaemia
leads to hyperplastic PT gland = tumour
= excess PTH and hypercalcaemia

198
Q

why might kidne failure cause hypo and hypercalcaemia

A

chronic kidney failure = low vit D = hypocalcaemia
low calcium = hyperplastic PT gland = tumour
= excess PTH and hypercalcaemia

199
Q

how do we check for parathyroid tumour in hypercalcaemia

A

check PTH levels
in normal, if calcium is high = low PTH
in tumour, if calcium is high = PTH also high

200
Q

what causes primary hyperthyroidism

A

benign tumour / hyperplasia

201
Q

if the pt has hyperthyroidism AND high PTH, what test do we do

A

24 hour urine calcium test
to determine if primary hyperparathyroidism OR FHH

202
Q

what are the two differential diagnosis for hypercalcaemia and high PTH and how do we differentiate

A

primary hyperparathyroidism OR FHH
24 hour calcium urine test < 0.01mmol/L = FHH
24 hour calcium urine test > 0.01mmol/L = primary hyperparathyroidism

203
Q

pt has hypercalcaemia. what tests do we do

A

PTH test
if high or normal = 24 hour urine test >0.01mmol/L is primary hyperparathyroidism and <0.01mmol/L is FHH
if low = malignancy,

204
Q

what is FHH

A

familial hypocalcuric hypocalcemia.
This is a kidney problem.
The body retains calcium at the kidneys, raising the blood levels. This causes the PTH to drop.

205
Q

what are the 4 consequences of primary hyperparathyroidism (oans)

A

BONEs (bone pain, osteoperosis, cysts in skull)
kidney STONES
physic GROANS - confusion
abdominal MOANS - constipation, acute pancreatisis

206
Q

pt has a cyst in the skull, feeling confused and constipation. What might be the cause

A

primary hyperparathyroidism = hyperclacaemia

207
Q

if a patient has hyperparathyroidism and is under 50, what do we do

A

surgery

208
Q

how do we treat hyperparathyroidism if mild

A

FIRST CHECK PTH levels
surgery if indicated (e.g. <50 years old or severe symptoms)
if not indicated, monitor 2 times a year

209
Q

how do we manage a hospitalised pt with hypercalcaemia

A

test blood for PTH!
normal IV saline solution for 5 hours
medications e.g. bisphosphonates (do XLA before this), cinacalcet, corticosteroids
Denosumab to prevent bone resoprtion
loop diuretics ONLY IF risk of overload

210
Q

what medications can be used for hypercalcaemia (5)

A

bisphosphonates (do XLA before this)
cinacalcet (calcium receptor agonist)
corticosteroids (vitamin D toxins)
Denosumab to prevent bone resoprtion RANK-L Ligand
loop diuretics ONLY IF risk of overload

211
Q

a patient is on cinacalcet , what are they being treated for

A

hypercalcaemia

212
Q

when do we give loop diuretics to a hypercalcaemic patient

A

if at risk of fluid overload from saline

3rd BDS IHD (14 decks)

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