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RACGP Exams Complete Deck > Endo4 > Flashcards

Endo4 Flashcards

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1
Q
A
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2
Q

What is the management of Cushings syndrome?

A

Treat cause

  1. For pituitary adenoma - surgery or radiotherapy
  2. Medically reduce cortisone by methyrapone (11 betahydroxylase blocker)
  3. Can be treated medically to reduce ACTH (Eg with bromocriptine)
  4. Last option is removing the adrenal gland with surgery
  5. Adrenal adenomas must be surgically removed
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3
Q

What is Nelson syndrome?

A

After bilateral adrenal gland removal, the pituitary forms an adenoma and secretes excess ACTH which causes hyperpigmentation of the body (Black pigmentation)

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4
Q

Where is ADH (Vasopressin Arginine) produced and stored?

A

Produced by hypothalamus and stored in posterior pituitary (So not completely shut down by pituitary dysfunction -still leak from hypothalamus)

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5
Q

What are key biochemical/physiological functions of ADH?

A

High plasma osmolality leads to ADH secretion.

It can also be stimulated by hypotension, hypovolaemia, hypothyroidism and cortisone.

It acts on V2 receptors in collecting ducts of kidney to activate aquaporins/water channels which absorb water and therefore reduce plasma osmolality

High plasma osmolality - stimulates thirst centre to drink more also

ADH in very high doses - acts on vascular V2 receptors and causes vasoconstriction

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6
Q

What pathologies of ADH are there?

A

Diabetes insipidus - cranial (Reduced ADH production) or nephrogenic (Reduced sensitivity of kidney to ADH)

SIADH - Inappropriately high ADH production

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7
Q

Symptoms of Diabetes Insipidus?

A

Polyuria, frequency and nocturia (15 L/day) with increased thirst

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8
Q

Key investigation findings in Diabetes Insipidus?

A

URINE OSMOLALITY is LOW - less than 600mOsm/kg

Serum Osmolalitly is high - 290mOsm/kg

Normal BGL

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9
Q

Diagnostic test for DI

A

water deprivation test

Serum osmolality increases but urine osmolality does not increase (not concentrating urine)

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10
Q

Can exogenous ADH fix Diabetes insipidus?

A

Cranial - yes, but not nephrogenic

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11
Q

What hormonal deficiency can mask DI?

A

Cortisone deficiency

With cortisone replacement you can start to see the symptoms of DI

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12
Q

What are the causes of cranial Diabetes Insipidus

A

Most commonly post pituitary surgery or post radiotherapy.

Other causes:

  1. Malignancies - Craniopharyngyoma, metastatic disease, hypothalamic tumour
  2. Infections - TB, Meningitis, cerebral Abcess
  3. Infiltrations - sarcoidosis, langerhans cell histocytosis
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13
Q

What are the causes of nephrogenic diabetes insipidus

A
  1. Renal disease
  2. Familial
  3. Drugs - lithium, glibenclamide
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14
Q

What happens in SIADH?

A

Increased ADH - therefore increased water reabsorption from kidney CD

Urine osmolality will increase

Serum osmolality will decrease

Diagnosis is made by Low serum sodium and low serum osmolality with High urine osmolality and urine sodium

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15
Q

Volume status in SIADH?

A

Patient is EUVOLAEMIC (not dehyrdated or overloaded)

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16
Q

What are causes of SIADH?

A

Think - Lung/CNS/Drugs

Infections: Pneumonia, Meningitis, TB

Tumours: Small cell lung cancer, thymus, pancreas, lymphoma, prostate, brain

CNS - Head injury/SDH/tumour

Drugs - Carbemazepine, cyclophosphamide Alcohol withdrawl

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17
Q

Treatment of SIADH?

A

Water deprivation - fluid restrict 1-2 Litres a day

Treat the underlying cause

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18
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A
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19
Q

A patient presents with symptoms and signs of Cushings syndrome but their serum cortisol/urinary cortisol are low - whats the explanation?

A

Suppression of the hypothalmo-pituitary-adrenal axis.

?Exogenous/Iatrogenic steroid use

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20
Q

What are the mechanisms of the main types of DM - 1, 2 and gestational

A

1- immune mediated destruction of beta cells - leading to insulin deficiency.

  1. A condition of relative insulin deficiency caused by progressive decline in beta secretion combined with insulin resistance
  2. Diabetes first diagnosed or recognised during pregnancy
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21
Q

What are other, uncommon, causes of DM?

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A

Pancreatic causes - Chronic pancreatitis, CF, Haemachromatosis

Genetic - monogenetic (HNF-1 Alpha deficiency) or defects in insulin action (eg Type A insulin resistance, leprechaunism)

Immune mediated uncommon but specific forms of diabetes ( eg stiff man syndrome, anti insulin receptor antibodies)

Congenital infection - CMV, and Rubella

Genetic syndromes with DM - (Downs Syndromes, Turner)

Hormonal - Acromegaly, Cushings, Phaeo,

PCOS

Drugs - Antipsychotics, corticosteroids and transplant drugs, ART, Dioxides

22
Q

What are comorbidities associated with TYPE 1 diabetes

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A

Can have autoimmune conditions

coeliac, thyroid and pernicious anaemia

AND have anti gad and anti islet cell antibodies

23
Q

Treatment goals with Type 1 DM

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A

Start Insulin early and institute Ketone checks when sick (Can have DKA)

Within 5 years - patient might have no endogenous insulin at all

24
Q

Type 2 DM comorbidities?

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A

Obesity

HTN

Dysplipidaemia

25
What is LADA?
Latent Autoimmune Diabetes in Adults Type 2 dx often without the cardiometabolic features Faster progression than usual Type 2 Dx supported by elevated Type 1 antibodies (anti- GAD, anti- Islet cell)
26
LADA management goals?
1. Early identification (check autoantibodies) 2. sick day management is same as type 1 (ketone check) as they can get DKA
27
A child or adolescent p/w DM and negative antibodies - Dx?
Diabetes Does not have to be antibody positive in all cases
28
When is C peptide used in DM testing?
It helps measure endogenous insulin production (endocrinologists might order this)
29
Clinical signs of insulin resistance?
Acanthosis nigricans Central obesity Hirustism Skin tags
30
Indications to commence insulin for a patient with DM at initial presentation?
1. DKA - (Type 1) - ED transfer urgently 2. DM - without ketones, but strongly suggestive of Type 1, may go into DKA - so commence 3. Patient presents asymptomatic but with significant hyperglycaemia - (Eg BGL over 18mmol or HBA1c over 10) For a pt with T2DM its usually possible to taper and stop insulin once symptoms and glucotoxicity have resolved and oral antihyperglycaemics are established.
31
Indications for hospital admission at initial presentation of DM?
1. DKA 2. Type 1 without DKA 3. Any of the following features at initial presentation - urgent t/f dehydration vomiting symptoms or signs of underlying systemic infection altered conscious state, delerium, confusion 4. If there's uncertainty about severity of patients condition - urgent referral
32
What are diagnositic sugar levels for DM based on?
Levels that can cause complications (Specifically retinopathy)
33
In a SYMPTOMATIC patient what are the criteria for DM?
Fasting BGL \> 7mmol/L Random BGL \> 11mmol/L HBA1c \> 6.5 % with symptoms is considered DM
34
Diabetic diagnostic criteria for ASYMPTOMATIC patients?
FBGL over 7mmol/L or a Random BGL over 11mmol/L - confirmed by a second FASTING BGL over 7mmol/L on a different day HBA1C over 6.5% confirmed with a second over 6.5% on a different day OR a FBGL over 7mmol/L OGTT with fasting over 7mmol/L or PPBS over 11mmol/L IF a single BGL is between 5,5 and 7 - follow up with OGTT
35
What is considered a positive OGTT?
FBGL over 7 or 2 hr reading over 11
36
How is Impaired fasting glucose on an OGTT defined?
FASTING - 6.1-6.9 with 2 hr less than 7.8
37
Management of Impaired glucose tolerance?
Lifestyle mods Refer to Allied health profs BP, BMI, lipids, Waist circ Problem areas in DM (PAID) tool **YEARLY DIABETES SCREEN**
38
Any conditions where an HBA1c result may over or underestimate
Conditions affecting erythropoiesis or red cell survival eg iron defs/ B12/ iron administration etc
39
Screening for T1 DM?
Not routinely recommended among family members
40
Screening of DM?
All non ATSI over 40 every 3 years using AUSDRISK ATSI over 18 every 3 years using AUSDRISK
41
Which patients require fasting BGL or HBA1c screening? Frequency of screening?
THREE YEARLY BLOOD SCREENING FOR THE FOLLOWING: AUSDRISK of 12 or more ALL ppl with history of previous CV event( AMI or stroke) Women with a history of GDM Women with PCOS Patients on antipsychotic drugs PPL aged over 40 with BMI over 30 OR hypertension Pacific Islander, Indian Subcontinent, Chinese with age over 35
42
What do you do if a patient has a HBA1c between 6.0 and 6.4?
REPEAT SCREENING IN ONE YEAR
43
If FBG is less than 5.5 or HBAIC less than 6?
Repeat testing in three years IF INDICATED
44
If FBG between 5.5 and 6.9?
DIABETES POSSIBLE - Perform OGTT to decide withether IFG, IGT, Diabetes
45
How is impaired glucose tolerance on an OGTT defined?
**2HR - 7.8 - 11mmol/**L, with fasting less than 7
46
What advice would you give a patient with impaired glucose tolerance or impaired fasting glucose
A person with IGT has an increased Macrovascular risk compared with the normal population Weight loss of 5-10% can reduce the progress of diabetes and improve glycaemic markers.
47
Any lifestyle modification advice for those with diabetes?
1. Weight reduction 5-10% 2. Balanced diet - limit salt to 6g/day, limit saturated fat intake, 3. Support smoking cessation and alcohol reduction to 2 SD a day 4. 150 -300mins moderate intensity exercise per week. Exercising on most days of the week. 5. Mediterranean diet has evidence of CV risk reduction benefit
48
When should you consider Type 1 Diabetes?
Ketosis/Ketonuria (+/-) Polyuria, polydipsia Weight loss or BMI \< 25g/m2 Less than 50 years old Personal and family history of Autoimmune disease Rapid onset of symptoms
49
Teenager presents with polyuria, polydipsia and weight loss. Initial management?
Assess - hydration state? Vomiting? _O/E_ Weight/GCS/Blood pressure/ Hydration state assessment _Bed side tests_ Urinalysis - Ph, Ketones Blood Ketones assessment (E.g using a bedside Optium meter ) If evidence of **blood ketones (GREATER THAN 0.6 mmol)** and **acidosis** contact the _diabetes specialist team at the nearest tertiary centre for advice._ Mainstay of managment will be - Call Ambulance for urgent transfer to Tertiary centre Securing Airway, breathing and circulation as per emergency protocols. Establishing IV access with large bore cannula **Monitor for signs** of **cerebral oedema** - headache, inappropriate slowing of the heart rate, change in neurological status, rising blood pressure, decreased oxygen saturation. Address fluid losses according to advice from diabetes team - usually parenteral rehydration - 0.9% Normal Saline 10ml/Kg Administration of insulin subcutaneously (dosage as advised by specialist team). (Often 0.25units/kg initially)
50
What are the signs of cerebral oedema in DKA?
headache, inappropriate slowing of the heart rate, change in neurological status, rising blood pressure, decreased oxygen saturation. REMEMBER Cushings triad of raised ICP (late) - Hyperbradybrady HTN, Bradycardia, Bradypnea(decreased resps)

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