Exam 2 Metab Emergencies

Question 1

What are causes of hypoglycemia

Answer 1

a) Delay in eating after taking insulin
b) poor caloric intake (dieting, vomiting)
c) increased or unusual physical exertion
d) increased physiologic stress (illness such as infection, trauma, emotional upset)
e) EXCESS EXOGENOUS INSULIN (addition of other DM meds esp sulonylureas in addition to insulin
f) impaired counter-regulatory hormone axis (glucagon, epinephrine, cortisol - don’t “kick in”)
g) variable absorption at injection site

Question 2

What is the definition and initial mgmt of hypoglycemia

Answer 2

def: <70 mg/dL
15-20 g oral CHO preferred
- 3 to 5 glu tab/candy or 1/2 c juice/non-diet soda

If NPO
IV dextrose 1 amp D50
Glucagon 1 mg IM or SC

Question 3

What can you expect in pt with hypoglycemia after initial tx of oral glucose, IV dextrose or IM glucagon (glucose has increased into normal range)

Answer 3

When blood glu increases into normal range, usually pt mental status normalizes (diaphoresis and tachycardia typically resolve)

• sometimes stroke like sx with focal neurological exam - these findings resolve with resolution of hypoglycemia
• keep observing pt

Question 4

sx of hypoglycemia include

Answer 4

irritability, diaphoresis and tachycardia, blurry vision and feeling weak

Question 5

What labs do you order if you are worried a pt might be hypoglycemic

Answer 5

Finger stick glucose
UA/microscopy
Urine hCG

Question 6

After hypoglycemia has resolved, what should we keep in mind about our pt?

Answer 6

the condition can reoccur!

• observe pt for time checking serial blood sugars, investigating why this happened and “fixing the problem”
• if the hypogly is bc of a sulfonylurea, admit the pt bc sulfonylurea half life is long, condition most likely will reoccur

Question 7

sx of DKA

Answer 7

Fruity breath odor
Tachycardia
Diffusely tender abd with involuntary guarding and hypoactive BS
vomiting and confusion
tachycardia, tachypnea, hypoTN, frequent urination
skin cool and dry
focal neurologic defects

Question 8

What are common lab values associated with DKA

Answer 8

• hypoNA (pseudo due to hyperglycemia)
• decreased bicarb
• increased BUN/Cr
• hypergly
• urine ketones
• acidotic ABG, normal PO2, low PCO2 (resp compensation)

**increased Anion gap (normal MUDPILES
methanol toxicity, uremia, DKA, Paraldehyde, iron toxicity/INH, lactic acidosis, ethylene glycol, salicylate

Question 9

What is MUDPILES associated with

Answer 9

causes of increased anion gap
Methanol toxicity
Uremia
DKA
Paraldehyde
Iron toxicity/INH
Lactic Acidosis
Ethylene glycol
Salicylate

Question 10

Ddx if: hyperglycemia, hypoTN, hypoNa, hypoK, dehydration, alter LOC, diffuse abd pain, acidosis, elevated anion gap

Answer 10

DKA

*first give IV fluids with isotonic saline

Question 11

What are the potential causes of hyperglycemic crisis in DM

Answer 11

DKA
Hyperosmolar hyperglycemic state (HHS) - aka hyperglycemic hyperosmolar non-ketotic state

*both precipitated by: illness, infection, trauma, surgery, MI, Insulin omission

Question 12

Etiology of DKA? s/sx

Answer 12

usually T1DM (old term IDDM) due to insulin insufficiency in the setting of a precipitant

s/sx dev over hr/d
*N/V abd pain, hyperventilation with fast and deep Kussmaul respirations, hypoTN/shock, dehydration, metab acidosis with increased anion gap, hypergly, serum ketones, Polyuria, polydipsia, wt loss

Question 13

How are DKA and DM dx related

Answer 13

DKA is the first sign of DM in 25% of T1DM, so lack of DM hx does not exclude dx

Question 14

DKA dx studies?

Glu, ketones, K, Na, Cl, bicarb, BUN/Cr

Answer 14

1) Glu generally >250 (usually at least in 400-500)
2) KETONES: urine and serum+
3) K+: high, low or normal - tends to be slightly high on initial labs but gen the body has sig K+ deficit (K tends to fall with hypergly tx, so watch closely and be prepared with supplement)
4) pseudohypoNa (corrected Na for glu formula)
5) Cl: low in anion gap
6) bicarb: LOW
7) BUN/Cr elevated (dehydration)
8) anion gap elevated
9) serum osmolarity elevated

Question 15

DKA dx studies continued

WBC, ABG, UA and CXR, EKG

Answer 15

elev WBC even in absence of infection (stress rxn, demargination)

ABG: acidosis overall

UA and CXR: may show infection (infection could precipitate DKA)

EKG: may show MI, electrolyte abn, arrhythmias (MI can precipitate DKA)

Question 16

What is the general primary goal in DKA tx?

Answer 16

stop the body from breaking down fats and using fat for fuel (ie ketones)

Question 17

Therapeutic goals DKA tx

Answer 17

a) restore circulatory volume
b) reduce blood glu
c) correct serum osm
d) clear serum ketones
e) correct electrolytes and anion gap
f) treat underlying causes

Question 18

outline the mgmt of DKA

Answer 18

1) ABCS
2) Isotonic saline (0.9 NS IV)
3) correct electrolyte disorders: follow K/Na, replete phosphate
4) **reverse acidosis and ketogenesis
5) control blood glu: insulin bolus IV (not always); continuous IV insulin infusion

Question 19

Fluid mgmt of DKA?

Answer 19

Give IV fluids aggressively

• 1-2 L NS in 1st hr (more if in shock, less if cardiomyopathy or HF)
• 250-500 mL/hr next 4 hr
• then reduce to 100-250 ml/hr
• monitor urine output (0.5-1 ml/kg/hr)**
• Change to 5% dextrose when blood glu <250 mg/dL – goal is to reverse ketogenesis not attain normoglycemia)

Question 20

How do we treat DKA acidosis

Answer 20

Give bicarb? generally bicarb NOT used to treat pt in DKA bc would further drive K into the cell (hypoK!)

*gen rule: let them be acidotic and focus on correcting the ketogenesis, only give bicarb if hyperK and want to drive K into the cell

Question 21

what are complications of using bicarb to treat acidosis

Answer 21

hyperNa, hypoK, paradoxical CSF acidosis and residual serum alkalosis

can lead to SEVERE CEREBRAL EDEMA and brain damage (first discovered in children)

Question 22

When is it appropriate to use Bicarb to treat acidosis?

Answer 22

when significant hyperK is evident

*bicarb can be livesaving to lower serum K by pushing K into the cells

Question 23

What is the mainstay of reversing Ketoacidosis

Answer 23

Fluid administration and insulin

• with insulin present, glu enters cells and body will d/c lypolysis
• blood glu will lower and ketones will clear

Question 24

When glucose normalizes after DKA (no longer hypergly, how should you approach the insulin infusion

Answer 24

it may seem sensible to stop insulin infusion at this time, but if the anion gap is still elevated, Insulin admin MUST CONTINUE
*it is the presence of insulin that stops the lipolysis

Question 25

Etiology of HHS

Answer 25

Mainly T2DM, typically in presence of precipitant (infection, MI, other stressors - often in older nursing home pt)

Question 26

S/sx HHS

Answer 26

s/sx: insidious (d to wk) onset, weakness, polydipsia, polyuria, dehydration, alter LOC *no abd pain or kussmaul respirations (bc no ketogenesis/acidosis) but may have an even higher glucose than DKA

Question 27

Pathophysiology of HHS

Answer 27

* Hyperglycemia then glycosuria then dehydration * Dehydration to hemoconcentration (results in worsening hyperglycemia; Glu 500+) * Dehydration (plasma osm >320) often 5-10 L deficient * relative insulin deficiency (insufficient to prevent hypergly and glycosuria but sufficient to prevent lipolysis and ketogenesis; absence of ketones/no acidosis)

Question 28

Tx of HHS

Answer 28

Fluid & electrolyte replacement - NS for circulatory collapse, - then .45% NS - once blood glu <250, use 5%D in .5 NS or .9NS Insulin IV - if fluid replacement alone is inadequate to decrease glucose - transition to SQ - transition to home regimen or optimize tx TREAT UNDERLYING PROBLEM

Question 29

What is the most common irregularly irregular rhythm

Answer 29

A fib *irregularly irregular rhythm associated with tachy = a fib with RVR (rapid ventricular response)

Question 30

Etiology and dx studies for thyroid storm

Answer 30

Catecholamine binding sites increased (heart and nerve tissues; increased sensitivity to circulating catecholamines) Dx: TSH low, FT4, FT3 high

Question 31

H&P typical findings for thyroid storm

Answer 31

All the normal hyperTH sx plus" - hypermetab (wt loss/diarrhea) - excessive adrenergic response - hyperpyrexia - a fib with possible HF - shock, coma, death

Question 32

Tx of thyroid storm

Answer 32

``` ABC B blocker (treat tachy and/or a fib) PTU and/or methimazole ASA/tylenol Fluids Electrolytes Nutritional support cooling blanket ```

Question 33

How do PTU and methimazole work to treat thyroid storm

Answer 33

PTU: decreases TH synthesis and blocks conversion of thyroxine (T4) to T3 Methimazole: decreases TH synthesis (no inhibition of peripheral conversion) *in contrast to PTU, methimazole does NOT sig inhibit T4 to T3 conversion

Question 34

What is myxedema Coma? cause? seasonality?

Answer 34

Rare complication of hypothyroidism * severe deficiency in TH leads to encephalopathy * winter mth after cold exposure * other precipitating events: CVA, surgery, trauma, meds, infection

Question 35

What are cardinal features of myxedema coma? onset and population at risk?

Answer 35

``` Hypothermia, hyporeflexia, CNS depression/coma, bradycardia, slow verbal responses ``` onset: may be rapid or insidious (elderly at highest risk)

Question 36

What is myxedema vs pretibial myxedema?

Answer 36

Myxedema: puffiness of hands and face; thickened nose, swollen lips, and enlarged tongue secondary to nonpitting edema with abn deposits of mucin in the skin and other tissues (mucin prevent pitting) "pretibial myxedema" is an uncommon skin disorder that occurs not in cases of hypoTH, but in HYPERTH, usually Graves (pretibial is misnomer bc can occur other places)

Question 37

What are causes of hyperglycemia

Answer 37

Illness, infection Trauma, surgery Myocardial Infarction Insulin Omission

Question 38

What is the mainstay of Treating acidosis (ketoacidosis)

Answer 38

FLUID AND INSULIN * with insulin, glu will enter cells and body will immediately dc lipolysis as a source for fuel * blood glu will lower and ketones will clear

Question 39

what is the prognosis and dx of myxedema coma? when should we suspect it?

Answer 39

Mortality 60-70% (tx drops to 15-20%) * high bx not easy to dx.. need high level of suspicioun * supsect when clinical manifestations of hx of hypoTH accompanied by disturbances of consciousness, hypothermia, hypoventilation, hypoTN

Question 40

what dx studies suggest myxedema coma

Answer 40

CMP: hypogly,hypoNa TSH: high FT4/3: low or undetectable CT head: norm unless trauma precipitated CXR: normal unless pericardial effusion or pneumonia precipitating event EKG: BRADYCARDIA, FLATTENING or inversion of T waves, possible conduction abn AG: HYPOXEMIA with HYPERCARBIA (if hypoventilation)

Question 41

Mgmt of Myx coma

Answer 41

``` ABC TH: T4 (T3 alone not rec) Glucocorticoid (given until AI r/o) IV fluids isotonic Correct electrolytes Rewarming blankets Find precipitating cause *slow recovery (metab abn take time) ```

Question 42

Thin male, responsive to pain, no evidence of head trauma, Lungs CTA bilat, heart mild tachy no MRG, weak peripheral pulses Hemoccult neg, no masses, no LE edema

Answer 42

HUGE ddx this is AI though *not enough cortisol produced by adrenal glands ADDISONS

Question 43

Primary vs secondary vs tertiary AI

Answer 43

Primary: problem at adrenal gland (addisons) Secondary: at pituitary (ACTH release inhibited) - often panhypopituitariasm bc isolated ACTH def rare Tertiary: supppression of HPA axis (usually due to w/drawal of steroids)

Question 44

What causes acute adrenal crisis

Answer 44

may result from acute exacerbation of chronic insufficiency usually sepsis or surgical stress can be caused by adrenal hemorrhage (ex septicemia induced waterhouse friderichsen syndrome fulminant meniningococcemia), anticoag complicaitons or congenital abnormalities ,

Question 45

Mgmt of adrenal crisis

Answer 45

ABCs, IV fluids, correct electrolytes HYDROCORTISONE, mineralocorticoic (Florinef) if needed, identify/treat underlying cause

Question 46

Acute adrenal crisis: suspect bacterial etiology (sepsis)

Answer 46

culture and then empiric broad spectrum abx *note: if any reason to suspect adrenal crisis, treat immediately with hydrocortisone

Question 47

When should we think of adrenal crisis

Answer 47

shock oterhwise unexplained and inadequate response to vasopressors and volume replacement