Endocrine Flashcards
Triggers for DKA
New onset T1DM Infection Inadequate insulin Surgery MI Pancreatitis
Drugs (Corticosteroids and thiazides, antipsychotics)
Chemotherapy
Psychosocial (EtOh, illicit substance use, eating disorders)
3 criteria for diagnosis of DKA
Hyperglycaemia
Ketonaemia
Acidaemia (from ketones)
What is DKA?
Occurs in diabetics - excessive serum glucose can’t be taken up into cells due to lack of insulin, so body is essentially starved and burns fats to produce energy which produces ketones as byproduct (acetone, gives fruity breath)
Symptoms of DKA?
Polydipsia, polyuria \+/-nausea, vomiting; leathery, anorexia; Altered conscious state/confusion, drowsiness; diffuse abdominal pain
Kussmaul hyperventilation (deep breathing)
What effect does DKA have on serum K?
How do you treat this?
Serum K may appear high despite an actual total body K loss. This is due to K shift out of cells into the serum due to insulin deficiency, and a large part of this shifted K is lost in the urine + vomiting can lose K + ketoacids are excreted in urine along with Na/K.
If K is low, add KCl to saline fluid bags.
K may also be normal or high. If high, do not give KCl in saline. Normal saline will cause K to be taken up into cells, as will insulin.
What effect does DKA have on plasma na?
How to manage this?
NA tends to be low due to the dilutional effect of water shifting from intra to extracellular space. However, water is lost in large amount in the urine due to polydipsia, which counter acts the dilution effect, so hyponatraemia tends to be mild
Give lots of 0.9% saline fluid (2 large bore cannulas) -> will cause Na to rise as fluid is taken up into cells
Management for Ketoacidosis
- Resus (ABC)
- Fluid (IV Saline)
- Electrolytes (K) - if K initially low, replace K before giving insulin because insulin will cause K to move into cells and the K will become even lower. If K normal, give at same time as insulin. If K high, do not give K but monitor it hourly.
- Insulin (causes K to move into cells)
- 5% Dextrose/glucose if
What electrolytes may need to be replaced in DKA?
K
Bicarb
Phosphate
Hyperglycaemic hyperosmolar state
Definition
Higher mortality risk and rarer than DKA.
HHS most commonly occurs in elderly patients with type 2 DM who have some concomitant illness that leads to reduced fluid intake. Infection is the most common preceding illness, but many other conditions can cause altered mentation, dehydration, or both.
HHS is characterized by hyperglycemia, hyperosmolarity, and dehydration without significant ketoacidosis
Hyperglycaemic hyperosmolar state
SX/signs
Severe hyperglycaemia Blood osmolarity high Profound dehydration Minimal ketosis or KA Depressed sensorium/coma (neurological deficits)
Hyperglycaemic hyperosmolar state
Treatment
Hypo-osmolar saline (0.45% rather than 0.9%)
Insulin
K
Monitor urine output and CVP if indicated
Prophylactic heparin
Treatment of hypoglycaemia
If conscious: oral fluids containing sugar or glucogel
If unconscious: 1mg IM/SC glucagon or IV 50% dextrose
Followed by oral carbs (sandwich) when conscious
Reassess glucose 20-30min later
Reason for hypoglycaemic incidence
Too little to eat Too much insulin Too much exercise Other medications (sulfonylureas) Renal failure
How to avoid hyper/hypoglycaemic emergency
DKA/HHS:
- never omit long-acting insulin (lantus, levemir), if you are T1
- Education re management when sick (monitor ketones, supplemental short-acting insulin regimes) -> T1D usually need more insulin than usual when unwell
Hypo:
- always carry form of sugar on you (lollies, juice, jellybeans)
- appropriate adjustment of glucose lowering therapies to prevent it happening again
investigations to perform for foot ulcer
Swab for MCS
Ankle brachial index
Basic bloods (WCC, CRP) +/- blood cultures
XR foot (exclude osteomyelitis)
Doppler USS and/or CT angiogram lower legs
Examination - foot ulcer
Colour
Temperature
Cap refill
Palpate pedal pulses and popliteal pulses (?femoral a stenosis)
Describe ulcers - borders, colour, exudate
Probe to bone (bone exposure indicates osteomyelitis)
Management of diabetic foot ulcer
Wound care and dressings Podiatry IV antibiotics Surgical debridement Reduce weight bearing forces Tight glycemic control!
Causes of hypothyroidism
Primary:
- Autoimmune (hashimoto’s)
- Iatrogenic (due to I^131, thyroidectomy, external irradiation of neck)
- Drugs (I, contrast, amiodarone, Li antithyroid drugs)
- Congenital (absent thyroid, dyhormonogenesis)
- Dietary I deficiency
Transient:
- post partum thyroiditis
- subacute thyroiditis
- withdrawal of thyroxine treatment
Secondary:
- Hypopituitarism
- Hypothalamic disease
- TSH deficiency/inactivity
What tests should be done to investigate thyroid function?
Blood TSH (if high, confirm T4)
Consider thyroid US if palpable goitre
Anti-TPO and Anti-TG antibodies (hashimoto)
Anti-TSH (Graves)
DO NOT need nuclear scan (unless they are thyrotoxic or have solitary nodule on U/S and want to know if it is hot or cold)
Treatment for hypothyroid
Thyroxine (needs to be taken separately from Iron, Ca, antacids which decr T4 absorption)
Adequate dietary Iodine
recheck TFTs after 6 weeks and adjust t4 dose if necessary
Causes of hyperthyroidism
- Graves
- Toxic nodular goitre (multinodular or solitary adenoma)
- Iodine induced (radiographic contrast, amiodarone)
- Factitious (too much T4 med)
- Transient (thyroiditis)
- Hypersecreting tumour within thyroid
What genes is T1DM linked with?
HLAD3 and D4
Pathophys of T1DM
Autoimmune destruction of insulin-secreting pancreatic beta cells, requiring patients to take exogenous insulin
What antibodies are associated w T1DM?
Islet beta cell antibodies (ICA)
Anti-glutamic acid decarboxylase (GAD)