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Complex Care 2 > Endocrine and Automimmune > Flashcards

Endocrine and Automimmune Flashcards

1
Q

Where is insulin produced in the body?

A

It is produced by the beta cells in the Islet of Langerhans in the pancreas.

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2
Q

What are the risk factors for developing Type 1 Diabetes?

A

Hx in the parent
AMA
Mother with hx of preeclampsia
Other autoimmune diseases

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3
Q

What are the symptoms of Type 1 Diabetes?

A 
Hyperglycemia
Polyuria
Polydipsia (excessive thirst)
Lipidemia
Polyphagia (excessive appetite)
Glycosuria
Ketoacidoses
Ketouria
Macular degeneration
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4
Q

What is the normal level should a fasting or random BGL?

A

Below 5.5

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5
Q

What level of fasting and random BGL is indicative of diabetes?

A

Fasting >= 7

Random >= 11.1

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6
Q

At what level of fasting and random BGL should an OGTT be done to confirm diabetes?

A

Fasting 5.5-6.9

Random 5.5 - 11

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7
Q

What are the risk factors for Type 2 diabetes?

A 
AMA > 45years
Overweight/obese
Hypertensive
CVD
Hx of GDM
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8
Q

What are the symptoms of Type 2 diabetes?

A 
Polyuria
Polydipsia
Polyphagia
Weight loss
Recurrent yeast infections
Recurrent UTI
Blurred vision
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9
Q

What are the long term complications of diabetes?

A 
Blindness
Renal disease
Nerve damage
Amputation
CVD: Stroke, Heart attack, loss of circulation arms/legs
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10
Q

How is diabetes treated/managed in pregnancy?

A 
Preconception counselling for Type 1
Strict blood glucose monitoring/control
Close medication management
Folate supplementation
Monitor fetus for teratogenic affects
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11
Q

What is thyrotoxicosis?

A

Excessive thyroid hormone production. Hyperthyroidism is one cause.

Graves disease is the most common cause (95%)

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12
Q

What medications are used to treat hyperthyroidism?

A

carbimazole or propylthiouracil (PTU) (the latter preferred in pregnancy). Both are Cat C drugs

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13
Q

What are the symptoms of Graves disease?

A 
Excessive perspiration
raised metabolic rate
Unexplained weight loss
rapid irregular HR
palpitations
hypertension
nervousness/agitation
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14
Q

How is hyperthyroidism treated?

A

Outside of pregnancy - surgery and radioactive iodine.

This can’t be done in pregnancy so tend to manage with PTU (blocks organification of iodine - essential step in making thryoid hormone) (can also be used when breastfeeding).

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15
Q

What are the two types of hypothyroidism?

A

Primary - impaired thyroid tissue

Central - Pituitary or hypothalmic

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16
Q

How is hypothyroidism diagnosed? What are the symptoms?

A

Elevated TSH with low Free T4

Majority have few or no symptoms but may include:
constipation,
weight gain / low basal metabolic rate,
thick/dry skin,
feeling cold,
oedema,
puffy eyes,
lethargy,
mental sluggishness / cognitive impairment,
alopecia,
Ataxia - lack of voluntary coordination of muscle movements that includes gait abnormality

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17
Q

How is hypothyroidism treated?

A

Thyroxine. (Cat A drug) 50 - 150 mircrog/day, with dosage increasing in pregnancy usually (25-50%).

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18
Q

What are the risks with hypothyroidism?

A

Gestational hypertension 2- 3 times more common
LBW
Psychomotor retardation
Infertility or increased risk of m/c or prolonged pregnancy

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19
Q

What should you consider when administering opiods to a woman with hypothyroidism?

A

They are more sensitive and so normal dosage may cause unconsciousness or death. Use cautiously.

20
Q

Myxoedema coma is a rare complication of ________?

A

undiagnosed or chronically untreated hypothyrodism. Presents with loss of conciousness with hypothermia, hypoventilation and bradycardia.

21
Q

What are the management considerations for hypothyroidism?

A

Regular bloods to monitor TSH and fT4
Monitor fetal growth - especially if hx of IUGR
Monitor for gestational hypertension

No special considerations in labour

Postpartum - reduction in thyroxine needed
Also follow up for baby - screening!

22
Q

What are the symptoms of hyperthyroidism?

A 
Heat intolerance
Weight loss
Insomnia
Agitation
Tremor
Sweating
Tachy and rebounding pulse
Diarrhea
Oligo or amenorrhea

Some of these usual in pregnancy so difficult to diagnose. Confirmed by raised fT4 and low TSH.

23
Q

What is Grave’s disease?

A

An autoimmune disease where auto-antibodies attack the TSH receptor causing high ft3 and ft4 which causes endogenous TSH to fall.

24
Q

What are the management considerations for hyperthyroidism?

A

Regular bloods to monitor fT4 and TSH
Serial growth scans for baby
Regular assessment for fetal tachycardia

Managed as high risk in labour with continuous CTG monitoring

Postpartum - addition obs, particularly pulse
Monitor baby for signs of goitre
Signs of neonatal thyrotoxicosis - weight loss, jitteriness, tachycardia, irritability, poor feeding

25
Q

What is obstetric cholestasis?

A

A pregnancy complication that affects the liver causing abnormal LFTs or raised bile acid levels. Resolves spontaneously after pregnancy.

Arises 3rd trimester after 28 weeks, characterised by pruritis of palms with no obvious rash, dark urine, anorexia, malabsorption of fat and elevated bile acid levels.

26
Q

What are risk factors for obstetric cholestasis?

A 
Ethnicity
Family Hx of biliary disease
Hep C
Prior OC
multiple gestation
AMA >35
27
Q

What is thought to cause obstetric cholestasis, and how does it impact the pregnancy?

A

Genetic hypersensitivity to oestrogen

Unexplained stillbirth?

Bile acids cause chronic uteroplacental vasoconstriction, fetal hypoxia and babies at risk of meconium aspiration.

28
Q

Management considerations with obstetric cholestasis?

A

Any woman with itching - refer for LFTs
Increased fetal surveillance with growth scan, doppler studies, AFI and CTG.
Early planned delivery at 37 weeks as IUFD rate of 7% in one study with 90% occuring after 37 weeks.

29
Q

Treatment of obstetric cholestasis?

A

Ursodoxycholic acid can be given (a type of bile acid) to address itching and balance biochemistry.

Dexamethasone (corticosteriod)
Vitamin K - OC can result in fat malabsorption so can be deficient in Vit K as is fat-soluable.
Antihistamines

Comfort measures - cool baths, loose clothing, skin lotions

Postpartum - avoid OCP with oestrogen.

30
Q

What is PUPP?

A

Pruritic Urticarial Papules and Plaques of pregnancy rash - usually third trimester.
Comes with severe itch in 80% of cases
Associated with weigh gain, primips and marked striae
No increase in fetal mortality.
Treatment - skin lubrication and topical antipruritics.

31
Q

What is systemic lupus erythematosus?

A

Inflammatory disease where immune system attacks it’s own tissues (autoantibodies to connective tissue), causing severe fatigue and joint pain.

90% in females
40% of people with SLE ALSO have APS.

32
Q

What happens to SLE in pregnancy?

A

1/3 improve, 1/3 stable, 1/3 worsen

Increased risk of gestational hypertension
Risk of preeclampsia
IUGR
preterm birth
IUFD (8% in 2nd and 3rd tri)
Miscarriage (increased risk 40 - 80%)
Congenital abnormalities
33
Q

What triggers a flare in SLE?

A

Infection, sunlight or increases in oestrogen.

34
Q

What are the symptoms of SLE?

A 
Classic butterfly rash on cheeks
Weight loss
fatigue and headaches
fever with flu-like symptoms
arthralgia
35
Q

Considerations for SLE in pregnancy?

A

Depends on severity of disease and if there is a “flare”.

Note - can have false positive for syphilis

Baseline bloods FBC, U&E, LFT, platelets, antibodies
Baseline proteinuria
Medication review required - change to NSAIDS, or corticosteriods (disease flare)? Aspirin for preeclampsia risk?

Fetal monitoring for congenital abnormalities and IUGR
Elective delivery if significant flare, preeclampsia, renal deterioration - care as per preterm infant!

NVB possible if no flare - continuous monitoring needed.

36
Q

Postpartum considerations for SLE?

A

Avoid oestrogen based OCP
Steriods for postpartum ‘flare’
Continue observations for 10 days to detect flare
Monitor for neonatal facial rash
Alert to psychiatric symptoms - don’t assume baby blues
Advise to avoid excess sunlight for baby - risk of neonatal lupus.

37
Q

What is antiphospholipid syndrome also known as?

A

Obstetric Lupus or Hughes Syndrome

It’s an acquired clotting disorder - can be primary or secondary (associated with an infection or other autoimmune disease such as SLE).

38
Q

How is APS diagnosed?

A

There must be one clincial feature, and one laboratory feature for diagnosis. For example: clinical feature = recurrent miscarriage, fetal death, venous or arterial thrombosis, autoimmune thrmobcytopaenia. Lab feature = presense of antibodies on blood test

39
Q

What are the antibodies associated with APS?

A

APA - antiphospholipid antibodies - bind to phospholipids in cell membranes and cause damage. If affects blood vessels - vasculopathy causing clots in narrowed and damaged vessels. Two types included are:
ACA - anticardiolipin antibody
LAC - lupus anticoagulant

Anti-Ro and Anti-La increase incidence of neonatal lupus and heart block on CTG.

40
Q

What does thrombophilia mean?

A

Thrombophilias are types of blood clotting disorders. APS is a type of thrombophilia

41
Q

What is the treatment for APS?

A

daily aspirin, LMWH, warfarin (but not in pregnancy as teratogenic)

42
Q

What risks are associated with APS in pregnancy?

A 
Preeclampsia
IUGR
recurrent miscarriage
preterm birth
abruption
HELLP
43
Q

Management of APS?

A

Booking in hx

Regular scans to detect IUGR
Aspirin and LMWH - clotting and preeclampsia
Frequent blood monitoring - FBC and platelets
Monitor for preeclampsia
Emotional support for possible poor outcomes

Labour - cease heparin, continuous CTG, anaesthetist consultation early, adequeate hydration - consider IV fluids?, TED stockings in labour, active management of third stage, prompt suturing of perineal trauma.

44
Q

Postpartum considerations for APS?

A

Be alert for thrombosis.

Thrombopropholaxis should be continued

45
Q

What is hashimoto’s disease?

A

Autoimmune condition that causes hypothyroidism - immune system attacks the thyroid gland causing inflammation and possibly destruction of the gland, limiting it’s ability to produce thyroid hormone.

Complex Care 2 (15 decks)

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