Endocrine Flashcards

You may prefer our related Brainscape-certified flashcards:
1
Q

previously diagnosed type 1 DM

A

est. based on hyperglycemia on multiple ED visits

refer to PCP for insulin dose adjustment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

tx of persistent hyperglycemia in T1DM

A

blood surgery level diary

every dose of insulin administered and type administered

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

undiagnosed diabetic ER

A

ER doc makes diagnosis with pt who fits criteria

confirmatory test needed and review of medical hx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

tx of undiagnosed diabetic in ER (stable)

A

12-24 hr f/u with PCP

if this is not possible, admit to tele

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

t1DM and glucocorticoid

A

develop hyperglycemia due to steroid tx

warning signs of hyperglycemia, seek close follow up with PCP and monitor glucose free.

add additional prandial doses of insulin )no need to increase basal insulin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

false glucose reading

A

icodextrin (peritoneal hemodialysis)

increased blood glucose levels with BEDSIDE reading

central lab glucose readings should be the ones that govern management

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

hypoglycemia value

A

plasma glucose <50 mg/dL

common in diabetics due to no surge of glucagon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

hypoglycemia blunting 2/2

A

age
BB
neuorpathy
repeat episode = autonomic dysfunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

evaluation of hypoglycemia

A

history and physical

emphasis on timing and administration of insulin relation to meals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

common causes of hypoglycemia

A
inadequate food intake 
infection 
change to regimine 
OD of medication or insulin 
BB toxicity 
renal failure 
ACS 
stress
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

s.s of hypoglycemia

A

drowsy, confused, dizzy, tired, cant concentrate or speak

tremor, sweating, anxiety, nausea, palpitations, shivering

hunger, weakness, blurred vision

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

alert pt hypoglycemia tx

A

glucose containing carbs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

unconscious pt hypoglycemia tx

A

Glucagon 1 mg IV, IM, SC

1 amp of D50 IV

then pt consumes meal or snack

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

glucagon emergency kit

A

T1DM family members carry for hypoglycemia

1 mg IM glucagon – 10-15 minutes onset then swallow oral glucose

can cause n/v

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

hypoglycemia discostino

A

not on long acting - discharged

on long acting - admitted for monitoring

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

DKA epidemiology

A

mc in insulin dependent DM (T1)

higher mortality in elderly and in coma or HoTN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

patho of DKA

A

cellular starvation 2/2 insulin deficiency and counter regulatory hormone excess

causes hyperglycemia, osmotic diuresis, preernal azotemia, ketone formation, wide anion gap metabolic acidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

insulin fxn

A

metabolism and storage of carbohydrates , fat, protein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

counter regulatory insulin hormones (4)

A

glucagon
catecholamines
cortisol
growth hormone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

hyperglycemia in DKA

A

due to excess production and underutilization of glucose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

counter regulatory hormones DKA cause

A

MC Glucagon

increased gluconeogenesis
breakdown of fats into free fatty acid and glycerol
proteolysis with increased amino acid level

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

lipolysis in DKA

A

free fatty acids that are released are broken down to ketone bodies and cause a metabolic acidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

osmotic diuresis in DKA

A

caused by persistently elevated glucose

causes volume depletion and worsened hyperglycemia and increased ketones

this activates RAAS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

vasodilation in DKA

A

despite volume depletion, prostaglandin activation is caused by adipose tissue breakdown

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

causes of DKA

A
reduced/skipped insulin injection 
infection
pegnancy 
hyperthyroidism 
substance abuse or medication 
heat 
CVA 
GI hemorrhage 
MI 
PE 
trauma or surgery
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

clinical manifestations of DKA due to

A

hyperglycemia
volume depletion
adcidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

clinical features DKA

A
polyuria, polydipsia 
increased ventilation 
HoTN 
weakness 
AMS 

poor turgor, fruity odor on breath, abdominal pain

28
Q

ventilation DKA

A

increased to try to counteract the metabolic acidosis

kussmaul respiration (increased rate and depth)

29
Q

MC presenting symptoms of DKA

A

tachycardia
HoTN

these are due to volume depletion

30
Q

main priority in DKA tx

A

give NS 1L IV bolus

31
Q

w.u. of DKA

A
accucheck
UA 
BMP 
12 lead EKG 
VBG
32
Q

DKA lab findings

A

serum glucose >250
anion gap >12
bicarb <15
pH <7.3

33
Q

hyperkalemia and DKA

A

due to extracellular shift of K (acidosis)
increased osmolarity due to hyperglycemia

if <3.3 – insulin therapy should not be started until K is managed

insulin will put K back in cell (dysrythma)

34
Q

ketones in DKA (3)

A

B-hydroxybutyrate
aceoacetic acid
acetone

35
Q

priorities of DKA tx

A
  1. volume first
  2. correction of K if needed
  3. insulin administration
36
Q

fluid administration DKA

A

fluids help increase volume and electrolytes and dilute glucose and ketone levels

1 L administered in first 30 (2L administered over 0-2 hrs)

NEXT: 2 L over 2-6 hrs and 2L more over 6-12 hrs

(total 6 L in 6-12 hrs)

37
Q

if blood glucose is 250 mEq, fluid admin…

A

5% dextrose in 0.45 NS + 20mEq KCL/L at infusion rate of 250 mL/hr thru second IV line

38
Q

Potassium and DKA

A

pts in DKA have potassium DEFECIT but the lab results are high

if initial K is 3.3 or lower (low) then the pt is severely depleted and must replace

life threatening derangement

39
Q

goals of K replacement DKA

A

maintain normal ECF K during acute therapy and replace the cell deficit in 24 hrs

if deleted rapidly – cardiac arrhythmia, respiratory paralysis, ileus, rhabdo

40
Q

DKA tx may cause K to fall bc

A

insulin promotes reentry into cell
dilution of ECF
acidosis correction

41
Q

K correction in DKA

serum: >5.3

A

IV insulin drip with NO supplemental potassium

42
Q

K correction in DKA

serum: 3.3-4.0

A

IV insulin drip

IV of 0.45 NS + KCL 40 mq/L at 250 mL/h

43
Q

K correction in DKA

serum: 4.0-5.3

A

IV insulin drop

IV 2 of 0.45 NS + KCL 20 mEq/L

44
Q

K correction in DKA

serum: <3.3

A

HOLD insulin

0.45 NS at 250 mL/h + 60 mEq/L until K >3.3

45
Q

insulin drip in DKA

A

following 1 L of NS and K correction can start

low dose regular insulin drip 0.1 u.kg.hr

once starting to infuse, concentration decreases 50 mg/dL.h

stop once ketonemia and anion gap gone

46
Q

insulin loading dose in DKA

A

can be give in adults but NOT IN PEDS (can cause cerebral edema and death)

47
Q

acute complications of DKA

A

sepsis
loss of airway
MI
hypovolemic schok

48
Q

DKA complications related to tx

A
hypoK
hypophosphatemia 
ARDS
cerebral edema
hypoglycemia
49
Q

late DKA complications

A

recurrent anion gap metabolic acidosis
non anion gap acidosis
vascular thrombosis
fungal infection

50
Q

DKA and pregnancy

A

triggered at lower serum glucose levels

pregos have more vomiting and UTI –> triggers of DKA

leading cause of fetal loss (30% mortality)

51
Q

DKA prego patho

A

mom hyperglycemia - fetal hyperglycemia and death
maternal acidosis = fetal acidosis, decreased blood flow and oxygenation
maternal hypoK = arrhythmia in fetus and death

52
Q

pt population most likely to get HHS

A

debilitated pt with poorly controlled T2DM or undiagnosed T2DM

53
Q

HHS precipitated by

A

limited access to water

medical event/stressor

54
Q

development of HHS is attributed to 3 main factors

A
  1. insulin resistance and/or deficiency
  2. increased hepatic gluconeogenesis and glyconeolysis
  3. osmotic diuresis and dehydration
55
Q

HHS patho

A

increased serum glucose causes water in vascular space and GFR increase

kidneys unable to reabsorb glucose = osmotic diuresis

pt is unable to replace fluid loss = water deficit and profound volume depletion

56
Q

history of HHS

A

elderly w/comorbidities start to develop mental status changes

57
Q

medical conditions that predispose a patient to HHS

A

PNA
UTI
non compliance with DM meds

PE, hear related illness, mesenteric ischemia, MI, burn, renal, CVA, rhabdo

58
Q

diagnosis of HHS

A

severe hyperglycemia (>600 mg glucose) with negative ketones

elevated osmolality of >315 mOSM/kg
arterial pH > 7.3

59
Q

serum osmolality in HSM

A

> 300 (>320- lethargy)

60
Q

HHS tx

A

correction of hypovolemia
ID and tx precipitating causes
correction of electrolyte abnormalities, hyperglycemia, osmolarity

61
Q

complications of HHS

A

cerebral edema UNCOMMON

limit volume rate to <50 ml/kg in first 4 hrs

potential for hypoglycemia, hypokalemia and pulmonary edema if rapid fluid admin

62
Q

alcoholic ketoacidosis

A

acute cessation of alcohol consumption after chronic abuse

N/V and GI complaints

drinking + vomiting then decreased food and alcohol changes

63
Q

alcoholic ketoacidosis s/s

A

tachycardia, tachypnea, abdominal tenderness

n/v, abdominal pain

64
Q

diagnostic criteria for alcoholic ketoacidosis

A
serum glucose low-slight elevated 
binge drinking ending in n/v/decreased intake 
wide anion gap metabolic acidosis
positive serum ketone 
wide anion gap metabolic acidosis
65
Q

tx of alcoholic ketoacidosis

A

hydration (5% dextrose)

carbohydrates to reverse ketoacitosis (increase insulin and suppress glucagon release)

thiamine supplementation

replace electrolytes