Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

DOOS 2 > DM-Table 1 > Flashcards

DM-Table 1 Flashcards

1
Q

Type 1 DM

A

requires insulin, autoimmune destruction of pancreatic beta cells

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

Type 2 DM

A

Progressive, chronically over wt/obese pts, lifestyle modifications, insulin resistance and eventual shut down of beta cells eventually

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

What are some complications of DM?

A

Emergent hypoglycemia, hyperosmolar hyperglycemic syndrome(HHS-2) or DKA(children-1), microvascular and macrovascular damage, neuropathic damage

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

how does DM present?

A

polyuria, polydipsia, polyphagia,

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

How do you dx?

A

If with symptoms-random blood glucose >200mg/dL asymptomatic: fasting bg>=126mg/dLx2, oral glucose tolerance >=200, A1C>=6.5%

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

What is A1C?

A

Measure of glycosylated hgb- it gives a good idea of glucose control over past 3months

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

What are the 3 levels of A1C and how they differ in therapy?

A

=9%=Triple therapy(metformin+two other meds)

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

When is metformin contraindicated?

A

Renal failure, liver or lung disease d/t acidemia(lactic acidosis)

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

Cornerstone of DM2 therapy?

A

Metformin

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

What are other antihyperglycemic drugs?

A

Sulfonylureas (hypoglycemia/wt gain), thiazolidinediones (pioglitazone, rosiglitazone-EDEMA-wt neutral), GLP-1 agonist(CI-men2, medullary syndrome- exenatide, liraglutide-secretagogs- wt loss), DPP-4 inhibitors(sitagliptin, linagliptin-protein that increases endogenous GLP-1 preservation=secretagogues- wt neutral)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

When should secretegogues be discontinued?

A

S/sx of pancreatitis (nawing back pain-burrowing)

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

What are some ADRs of metformin?

A

Lacitic acidosis, GI upset

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

What PO anti-hyperglycemic drug causes wt gain?

A

Sulfonylureas- glipizide, gliburide, chlorpropamide

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

What PO anti-hyperglycemic drug causes water retention?

A

thiazolidinediones (pioglitazone, rosiglitazone)- don’t use in HF pts

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

What are wt neurtral PO anti-hyperglycemic drugs?

A

Thiazolidinediones, DPP-4, metformin

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

What subQ anit-hyperglycemic drug causes wt loss?

A

GLP-1 agonist (exenatide, liraglutide), CI: MEN2 and hx of medullary thyroid cancer

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

Muscle can take up glucose without insulin(T/F)?

A

True, this is why you should probably not inject insulin before working out…

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

DKA presentations?

A

Only occurs in type 1 dm, often no previous dx of DM1, s/sx: polyuria,polydipsia, N/V, malaise, fatigue, tachypnea, palpitations, abdominal pain, ALOC(altered conciousness)

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

HHS-hyperosmolar hyperglycemic state

A

more type 2 dm, older/infirmed or non-compliant patients

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

What is DKA?

A

Severe insulin deficiency- lipolysis occurs=ketone bodies, acidemia(anion gap will be high),

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

How do you dx DKA?

A

Clinical and labs: fingerstick glucose>250, UA+dipstick(glucose and ketones), CMP(hyperkalemia(glucose travels with potassium..), hyponatremia, low bicarb, high anion gap), CBC(left shift=infections), ABG(metabolic acidosis), EKG, serum hydroxybutyrate(high=monitor progress)

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

What often times percipitates DKA?

A

inflammatory process/drug use-cocaine/non-compliance

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

What is PE for DKA?

A

dry skin, dry mucous membranes, reduced skin turgor, hypotensive, tachycardic, confusion, ill-looking patient

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

What is DKA tx?

A

ADMIT: Based on ABCs: circulation(depleted fluids)=NS bolus(up to 5L given), administer normal insulin IV(monitor KqH), Hypokalemia(if

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

What are some electrical changes seen on EKG d/t hypokalemia?

A

Flat T waves, prominant U waves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is the underlying problem with HHS?

A

Profound dehydration, high glucosuria

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

What is clinical presentation of HHS?

A

ALOC, focal/global neurologic deficits, thirst polyuria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

How do you dx HHS?

A

clinical: fingerstick glucose(>600mg/dl), cmp, ua+ dipstick(high glucose), CBC, CSP, CXR(look for infection), EKG, CT, AZOTEMIA-d/t elevated BUN(less perfusion to kidneys)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is the tx for HHS?

A

ABC: Replenish fluid volume very first 1-2L of NS in first hr- get serial CMPs qH, once azotemia resolved, can start insulin, monitor K,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Hypoglycemia is recognized as?

A

Sympathetic activation(sweating, tremor, tachycardia, palpitations, anxiety, nausea, vomiting), blurred vision, behavioral changes, fatigue, ALOC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What are the normal levels for fasting blood glucose?

A

70-120mg/dL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is the dawn phenomenon?

A

increased insulin required in early morning dt GH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is the somogyi effect?

A

rebound hyperglycemia from night time hypoglycemia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What is the usual insulin to carb ratio?

A

1:15

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is the usual correction factor?

A

1:50

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What are rapid acting insulin?

A

lispro, aspart, apidra

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

what should you do to insulin when adding Pramlintide?

A

reduce pre-prandial insulin by 50%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

When should you screen children for DM2?

A

when BMI over 85th precentil, or wt over 120% of ideal,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What is metabolic syndrome?

A

3 of 5 criteria met (PHAT)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What are the ranges for metabolic syndrome?

A

BP>130/85, HDL cholesterol 102men/>88women, TG>= 150, Fbg >=110

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What are the characteristics of metabolic syndrome?

A

impaired lipids, impaired

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What happens when there is low blood glucose?

A

Glucagon is released by alpha cells of the pancreas

Liver releases glucose into the blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What happens when there is high blood glucose?

A

Insulin released by beta cells of the pancreas

Fat cells take in glucose from the blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

what are the types of DM?

A

Type I, II, gestational, other

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What is the cause of Type I?

A

Due to B cell destruction, usually leading to absolute insulin def

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What is Type II caused by?

A

d/t progressive insulin secretory defect on the background of insulin resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What are the other types of DM?

A

Monogenic diabetes- neotnatal, MODY

Dz of endocrine pancreas and drug/chemical induced

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What is MODY?

A

Dysregulation of glucose sensing or insulin secretion
AD mutation
Occurs beore 25
Insulin resistance and hypertriacyclglycerolemia absent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What causes gestational DM?

A

Rise in HPL and other hormones that contribute to insulin resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What is diabetes mellitus?

A

Metabolic disorder in which carbohydrate metabolism is reduced while that of proteins and lipids in increased

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

How is Diabetes diagnosed?

A

•Fasting plasma glucose (FPG) ≥ 126mg/dl
OR
•Symptoms of diabetes + casual plasma glucose ≥ 200 mg/dl
OR
•Oral glucose tolerance test (OGTT): 2-h postload glucose ≥ 200 mg/dl

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What needs to be taken into consideration with A1C?

A

Need to take into account age, race, anemia or hemoglobin issues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What are contraindications to A1C testing?

A

Use of plasma glucose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

When should you test for DM?

A

1) Adults overweight or obese and who have 1 or more additional risk factors for diabetes
2) all pts testing at age 45
3) repeat at a minimum of 3 yr interval if results are normal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What are the additional risks for overweight/obese diabetics?

A 
–Physical inactivity
–First degree relative with diabetes
–High risk race/ethnicity (AA, Latino, Native American, Asian American, Pacific Islander)
–Women who delivered a baby weight > 9 pounds or were diagnosed with GDM
–HTN (> 140/90 or on therapy)
–HDL cholesterol  250mg/dL
–Women with Polycysic ovarian syndrome
–A1C > 5.7% on previous testing
–Severe obesity or acanthosis nigricans
–History of CVD
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

When should you test for gestational diabetes?

A
  • Test for undiagnosed diabetes type 2 in pts with risk factors at first prenatal visit
  • test at 24-28 wks gestation in women with no hx of dm
  • screen women with GDM for persistent DM at 6-12 wk post partum and lifelong screening at least q 3 yrs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What is GDM associated with ?

A

Fetal macrosomia
Higher rate of pre-eclampsia
Mother is at risk for developing type 2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What puts women at very high risk for GDM?

A

Severe obestity, prior hx of GDM or delivery of LGA infants, presence of glycosuria, diagnosis of PCOS, or strong family hx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

When should women be screened for GDM?

A

Women at high risk as soon as pregnancy is confirmed

All other at 24-28wks of gestation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

How is GDM diagnosed?

A
  • Fasting ≥ 95 mg/dL
  • 1h ≥ 180 mg/dL
  • 2h ≥155 mg/dL
  • 3 h ≥ 140 mg/dL
  • Women with GDM should be screened for type 2 diabetes 6-12 weeks postpartum
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What are common comorbid conditions with diabetes?

A

Depression, OSA, fatty liver dz, CA, fractures, cognitive impairment, low testosterone in men, periodontal dz, and hearing impairment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

When should you monitor glucose on intensive insulin regimens?

A

Prior to meals and snacks, occasionally post-prandial, at bedtime, prior to exercise, when they suspect low blood glucose, after treating low blood glucose, and prior to critical tasks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

When should A1C be monitored?

A

At least 2x yr in pts that are meeting treatment goals

Quarterly in pts not meeting goals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What is the cause of type I diabetes?

A

Absolute insulin def

Autoimmune destruction of the B cells of the pancreas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What markers are present in type I diabetes?

A

Islet cell antibodies
Autoantibodies to insulin
Autoantibodies to glutamic acid decarboxylase( GAD65)
Autoantibodies to tyrosine phosphates IA-2 and IA-2B

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

What are risk factors for type I DM?

A

Strong genetic component, environmental factors
White
Other autoimmune disorders

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What are the 4 main features of the progression of diabetes type I?

A

1) pre-clinical period with the presence of immune markers
2) hyperglycemia after 80-90% of B cells are destroyed
3) honeymoon phase
4) established disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What is the clinical presentation of hyperglycemia??

A

Polyuria, polydipsia, polyphagia, wt los, fatigue, infection, blurred vision, poor healing, growth failure in children, N/V

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

What is the tx for type I DM?

A

Provide exogenous insulin to replace endogenous loss

  • insulin
  • pramlintide
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What are the types of insulin?

A
  • rapid acting
  • short acting-regular insulin
  • intermediate acting- NPH
  • long acting-basal insulin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

What are the rapid acting insulins?

A

Humalog, novolog, apidra

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

What are the short acting regular insulins?

A

Novolin, humulin R

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

What are the intermediate acting NPH?

A

Novolin and humilin N, Neutral protamine Hagedorn (NPH)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

What are the long acting basal insulins?

A

Levemir (detemir) and lantus (glargine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

What are the high insulin state effects?

A
  • liver: glucose uptake, glycogen synthesis, lipogensis
  • muscle: glucose uptake, glucose oxidation, glycogen synthesis, and protein synthesis
  • adipose tissue: glucose uptake lipid synthesis and TG uptake
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

What are the low insulin state effects?

A
  • liver: glucose production, glycogenolysis, ketogenesis
  • muscle: fatty acid, ketone oxidation, glycogenolysis, proteolysis and amino acid release, NO glucose uptake
  • adipose tissue: lipolysis and fatty acid release. NO glucose or TG uptake
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

What is the onset of insulin detemir(levemir)?

A

Onset 2 hrs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

What is the peak and duration of insulin detemir?

A

6 to 9 hrs (blunted)

and 24 hr duration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

What is the onset, peak, and duration of insulin glargine (lantus)?

A

Onset 4-5hrs
Peak none or blunted
Duration 22+ hrs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

What should you do before using NPH?

A

Roll or invert 10 times

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

What Is the onset, peak, duration of NPH?

A

Onset of 1-4hrs
Peaks at 6-10hrs
Duration of 12-18 hrs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Can NPH also be used as a basal insulin?

A

Yes if dosed multiple times a day

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

When should short acting regular insulin be injected?

A

30 min before eating

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

Onset, peak, and duration of short acting regular insulin?

A

Onset ½- 1 hr
Peak of 2-5 hrs
Duration of 4-6 hrs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

What insulin most closely mimics the bodys response to glucose absorption?

A

Rapid-acting insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

When should rapid-acting insulin be injected?

A

Immediately before eating

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

What is the onset, peak and duration of rapid acting insulin?

A

Onset: 5-15min
Peak: ½ to 1.5 hrs
Duration: 3.5 -5hrs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

What is the pre-mixed insulin basal/bolus?

A

-NPH+regular
70/30
-NPH-like insulin +rapid acting
-aspart protamine/aspart(novolog mix 70/30)
-neutral protamine lispro/lispro (humalog mix 75/25, or 50/50)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

What is the adverse effect of insulin?

A

Hypoglycemia- blood glucose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

What is hypoglycemia a result of?

A

Decrease of insulin, decreased or delay in meals, increase in exercise

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

What are the S/S of hypoglycemia?

A

Tremors, palpitation, sweating, excessive hunger, HA, mood changes, irritability, unconsciousness, and seizures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

How is hypoglycemia tx?

A

15g of glucose, wait 15min if still

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

What are sources of carbs?

A

½ cup of juice, 3 graham crackers….liquids are much faster acting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

What is hypoglycemia unawareness?

A

Secretion of glucagon and epi are blunted, reducing symptoms of hypoglycemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

How does admin affect absorption?

A

Rate of absorption varied by route and location
IV>IM>SC
Ab>arm>thigh>butt

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

What can pts do to help enhance absorption?

A

Rub injection site- blood flow enhances

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

How is most insulin stored?

A

Room temp for up to 28 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

What are the exceptions for insulin storage?

A

–Humalog Mix Pen: 10 days at room temperature
–NPH-Regular Mix Pens : 10 days
–NPH Pens: 14 days
–Novolog Mix Pen: 14 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

What does the insulin pump do?

A

Deliver microliter amounts of insulin continuously as a basal insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

When should the insulin pump be activated?

A

Before a meal to deliver a bolus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

What is pramlintide?

A

Synthetic analog of human amylin, which is co-secreted with insulin from the pancreas in response to a meal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

What are the 3 primary mechanisms of amylin?

A
  • suppress postprandial glucagon secretion
  • regulates the rate of gastric emptying
  • reduce food intake
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

Amylin is deficient in which form of diabetes?

A

Both I and 2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

What is the primary use of pramlintide?

A

FDA approved for I/II in pts on optimal insulin therapy who are sill not at goal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

What is type I dosing for pramlintide?

A

15mcg SC before meals

meals must be >30g of carbs or >250kcals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

What do you HAVE to do when starting a pt on pramlitide?

A

Reduce pre-prandial insulin by 50%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

What are CI/ precautions with pramlintide?

A

Gastroparesis, hypoglycemic unawareness, recurrent episodes of hypoglycemia in the last 6 mo, A1C >9%, poor adherence to insulin or self monitoring

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

What is the black box warning for pramlintide?

A

Hypoglycemia
Usually within 3 hrs of injection
This is why you have to reduce preprandial insulin by 50% at initiation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

What are other adverse effects of pramlintide?

A

Nausea, drug interactions, and delayed gastric emptying

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

What are the ADA guidelines for glycemic control of TypeI/II?

A

•A1C

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

What are steps for recommended therapy in diabetes type I?

A
  1. Use of multiple dose insulin injections
    –3-4 injections/day of basal and prandial insulin
  2. Matching prandial insulin to:
    –Carbohydrate intake
    –Premeal BG
    –And anticipated activity
  3. Use of insulin analogs as prandial insulin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

What is the standard of care in type I diabetes?

A
  • miminum of 4 injections
  • basal admin once/day typically at bedtime
  • rapid acting bolus given just before meals
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

What is initial insulin dosing based off of?

A

Weight

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

What is the max insulin units that can be absorbed or injected at one site?

A

50 units

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

What are the 2 parts to prandial insulin dosing?

A
  1. insulin to carb ration (I:C)

2. correction factor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

What is the typical starting I:C?

A

1:15

1 unit of insulin covers 15 g of carbs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

What is correction factor?

A

Number of mg/dL the blood glucose will drop after injecting 1 unit of rapid-acting or regular insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

What is a typical starting CF dose?

A

1:50

1 unit of insulin for every 50 mg/dL above 100

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

What is the 1500 rule using TDD to calculate the CF?

A

1500/TDD mg/dL the blood glucose will drop after 1 unit of insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

What are causes of fasting hyperglycemia?

A

Dawn phenomenon: increased insulin requirement late in the sleep cycle- nocturnal hyperglycemia
Somogyi phenomenon: nocturnal hypoglycemia followed by rebound hyperglycemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

When does the somogyi effect more often happen?

A

When intermediate insulins are used with dinner

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

How does the somogyi effect happen?

A

Happens when hypoglycemia causes the release of counterregularoty hormones hich stimulate hepatic glucose production which leads to rebound hypergycemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

When should you measure blood glucose levels of suspecting somogyi effect?

A

Btwn 2 and 4 am then again at 7am

–If they are 180-200 mg/dL rebound hyperglycemia may have occurred

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

What is the dawn phenomenon?

A

An increased insulin requirement in the early morning

About 1-3am d/t a surge of growth hormone relsease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

What is the cause of postprandial hyperglycemia (>180)? When does it occur? How is it treated?

A

Not enough insulin given with the meal
Happens 1-2 hrs after eating
Increase the pre-meal insulin dose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

How should the I:C be adjusted if the post prandial glucose is consistently >180?

A

Adjust by 2-5 grams of carbs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
127
Q

How should the I:C be adjusted if it is at 1:15 and the 2hr post prandial blood glucose levels are 210?

A

Increase to 1:12

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
128
Q

What are strategies to avoid hypoglycemia?

A
  • planned exercise: decrease pre-prandial insulin dose before the exercise
  • unplanned exercise: consume an additional 15-30g of carbs for each 30 min of exercise
  • might need to decrease pre-prandial insulin dose for the meal after exercising
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q

What should you always check during illness if your blood glucose is consistently over 240?

A

Urine ketones!

persistent is early sign of DKA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
130
Q

What are complications of DM I?

A

Hypoglycemia

Ketoacidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
131
Q

What are s/s of ketoacidosis?

A 
–Develop rapidly
–Fruity or acetone breath
–N+V
–Dehydration- typically 6L or more
–Polyuria
–Polydipsia
–Deep, rapid breathing
Lethargy, HA, weakness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
132
Q

What is the diagnostic criteria for ketoacidosis?

A

–Hyperglycemia (> 250mg/dL)
–Ketosis (anion gap > 10)
–Acidosis (arterial pH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
133
Q

How is DKA tx?

A

Reverse underlying metabolic abnormality
Rehydrate with NS at 1L/hr
Normalize serum glucose with regular insulin at 0.1-0.2 unit/kg/hr by CI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
134
Q

What is the pathophys of DM II?

A

Insulin resistance and relative insulin def

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
135
Q

What are the other physiologic issues that happen in Type II DM?

A

Reduced circulating levels of GLP-1
Loss of first phase insulin response post meal
Loss of amylin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
136
Q

What are risk factors for type II?

A
  • Physically inactive
  • 1st degree relative with diabetes
  • Minority ethnic groups
  • Gestational diabetes or delivering baby >9 lbs
  • Hypertension
  • HLD 250 mg/dL
  • Polycystic ovary syndrome
  • Previous impaired glucose tolerance (IGT) or impaired fasting glucose (IFG)
  • History of vascular disease
  • Psychiatric illness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
137
Q

When should you consider screening for DM?

A

Pts of any age if their BMI >/= 25kg.mg and they have additional risk factors for DM
If NO risk factors begin at age 45

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
138
Q

How often should screening be repeated?

A

Q 3 yrs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
139
Q

What indicate screening for type 2 DM in kiddos?

A

Overweight: BMI >85th percentile for age and sex, wt for height >85th percentile, or weight >120% of ideal for height
PLUS 2 of the following
Fhx in 1st or 2nd degree relative, ot white, signs of insulin resistance, GDM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
140
Q

When should testing in kiddos be done?

A

Start at 10 or onset of puberty

Test FPG q 2yrs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
141
Q

What is the definition of pre-DM?

A 
IFG= 100-125
IGT= 2hr post load glucose 140-199
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
142
Q

IFG and IGT indicate risk factor for what?

A

Diabetes and CV disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
143
Q

What is diagnostic for DM II?

A 
FPG >/= 126mg/dL                   
OR
Symptoms of diabetes + casual plasma glucose >/= 200 mg/dL
  OR
Oral glucose tolerance test  (OGTT): 
   2hr-postload glucose >/= 200 mg/dL
A1C>/= 6.5
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
144
Q

What is the preferred test for diagnosing DM?

A

FPG./= 126mg/dL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
145
Q

What are the 3 major metabolic abnormalities that contribute to hyperglycemia?

A
  • Defective glucose-induced insulin secretion
  • Increased hepatic glucose output
  • Inability of insulin to stimulate glucose uptake in peripheral target tissues.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
146
Q

What are some other causes of insulin resistance?

A

Cushings- excessive corticosteroids
Acromegaly- excessive GH
PCOS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
147
Q

What are the microvascular complications of DM?

A

Retinopathy, nephropathy, neuropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
148
Q

What are the macrovascular complications of DM?

A

Atherosclerotic CV diagnosis, dyslipidemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
149
Q

What is the A1C goal for adults in general? Why?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
150
Q

What are some ways to prevent DM in pts with IGT or IFG?

A

Wt loss of 7% body weight and increase PE to 150 min/week
Add 14g of dietary fiber/ 1000 kcal
Meds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
151
Q

What drugs have been studied for prevention of DM?

A

Metformin, rosiglitazone, acarbose, troglitazone, orlistat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
152
Q

How can DM be clinically managed?

A

Diet/ exercise are cornerstones of DM management regardless of severity and symptoms
Meds highly individualized

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
153
Q

What is the goal in clinical management of DM?

A

To improve symptoms of hyperglycemia, reduce onset & progression of microvascular and macrovascular complications, reduce mortality & improve QOL.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
154
Q

What are some ways to improve sugars and manage CV risk factors?

A

Smoking cessation, lipid management, BP control, and antiplatelet therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
155
Q

How often should glucose be self monitored?

A

If insulin injection: at least 3x/day

If oral: use to achieve glycemic goals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
156
Q

How often should A1C be monitored?

A

At least 2x yearly in pts at goal

Q 3 mo in pts who aren’t meeting goals or who have had a change in meds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
157
Q

What are the oral therapy options for DM II?

A

Biguanides- Metformin
Secretagogues- sulfonylureas
Short acting secretagogues- meglitinides
Insulin sensitizers- TZD, thiazolidinediones
Alpha-glucosidase inhibs
Dipeptidyl peptidase-4( DPP-4)inhib
Bile acid sequestrants
Colesevelam (welchol)
D2 agonists- bromocriptine
Sodium glucose transporter 2 inhib( SGLT2 inhib)- canaglifozin, dapagliflozin, empagliflozin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
158
Q

What is the MOA of metformin?

A

Decreases: production of hepatic glucose production, intestinal glucose absorption
Increases: peripheral glucose uptake and insulin sensitivity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
159
Q

What are the clinical used of metformin?

A

Works best in pts with significant hyperglycemia
First line in type 2 DM pharm tx
Shown to decrease CVD in DM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
160
Q

What are the ADRs of metformin?

A

GI- diarrhea, ab bloating, nausea
Vit B12 def
Lactic acidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
161
Q

How can GI affects be minimized?

A

Take with food, titrate dose at weekly intervals to minimize

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
162
Q

What is an ADR of metformin that is actually beneficial?

A

Hypoglycemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
163
Q

What needs to be monitored and when if your pt is taking metformin?

A

SCr at baseline
FPG at 2 weeks
A1C at 3 mo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
164
Q

What is the pathophys behind metformin associated lactic acidosis?

A

Increased production of lactate n the intestine leads to increased portal lactate concentrations which decreases liver pH, decreasing lactate metabolism and leads to accumulation in the blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
165
Q

What are CI with metformin?

A

Renal impairments, acute or chronic metabolic acidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
166
Q

What are the precautions of metformin?

A

Radiocontrast studies, age>80 unless normal GFR, hypoxic states, alcoholism, heart failure requiring pharm tx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
167
Q

What are some benefits of metformin?

A
  • no weight gain
  • no hypoglycemia as a monotherapy
  • inexpensive
  • approved an monotherapy and a combo therapy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
168
Q

What is the MOA of sulfonylureas?

A

Direct stimulation of insulin release from viable pancreatic beta-cells thus reducing blood glucose levels
Blocks ATP-sensitive K+ channels, resulting in depolarization and Ca++ influxrelease of insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
169
Q

Which generation of sulfonylureas are no longer used?

A

Generation 1 because of the higher risk of hypoglycemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
170
Q

What are the 2nd generation sulfonylureas?

A

Glyburide, Glipizide, Glimepiride, Gliclazide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
171
Q

What are the clinical used of 2nd generation sulfonylureas?

A

Mild to moderate Type 2 diabetes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
172
Q

What are the ADRs of 2nd gen sulfonlyureas?

A

Hypoglycemia, weight gain, muscular weakness, dizziness, confusion, skin rash, photosensitivity, blood dyscrasias, cholestatic jaundice

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
173
Q

What are the specific directions or risks with glyburide?

A

Admin with breakfast or first main meal
Greater risk of hypoglycemia d/t longer half life
Don’t use if CrCl

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
174
Q

What are directions and risks with Glipizide?

A
  • Administer 30 min before first main meal

- Not recommended if CrCl

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
175
Q

What are specifics for Glimepiride?

A
  • Administer with first main meal

- Not recommended if CrCl

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
176
Q

What affects the absorption of sulfon?

A

Reduced GI absorption if blood glucose is >250mg/dL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
177
Q

What needs to monitored if your pt is on sulfonylureas?

A

FGP- 2 weeks

A1C- in 3 mo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
178
Q

What are CI/ cautions for sulfonylureas?

A

Cross sensitivity to sulfa, higher risk with hypoglycemia in pts with renal or hepatic dz, avoid with ETOH, CI in pregnancy since it can cross the placenta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
179
Q

What are the drug interactions with sulfonylureas? what are they doing?

A

May potentiate hypoglycemia via reduced hepatic metabolism, decreased urinary excretion or displacement from plasma proteins

  • Sulfonamide antibacterials
  • Propranolol
  • Salicylates
  • Phenylbutazone
  • ETOH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
180
Q

What is the MOA of the short acting secretagogues (meglitinides)?

A

Stimulate insulin release from pancreatic beta cells- increases insulin secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
181
Q

When should meglitinides be taken?

A

With meals to target postprandial glucose levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
182
Q

What are the meglitinides?

A

Repaglinide and nateglinide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
183
Q

What is repaglinide approved for?

A

Monotherapy or with metformin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
184
Q

When should repagalinide be given?

A

Taken before meals 3x daily

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
185
Q

What is nateglinide approved for?

A

Monotherapy or combo with metformin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
186
Q

What is the difference with nat and rep?

A

Nate has a faster onset of action and shorter duration of action than rep, less A1C reduction than rep
Also take 3x daily before meals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
187
Q

What are the ADRs of meglitinides?

A

Hypoglycemia and weight gain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
188
Q

What do you need to be monitoring if your pt is on meglitinides?

A

FGP at 2 weeks
Postprandial glucose at initiation
A1C at 3 months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
189
Q

What are the TZDs?

A

Rosiglitazone and pioglitazone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
190
Q

What is the MOA of TZDs?

A

regulate glucose metabolism resulting in increased insulin sensitivity in adipose, liver and skeletal muscle
they REQUIRE INSULIN for action

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
191
Q

Whats shouldn’t you give with rosiglitazone?

A

Exogenous insulin! Will lead to edema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
192
Q

About how long does it take for the biological effect of TDZs to be seens?

A

4 weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
193
Q

What are the CV effects of pioglitazone?

A

HDL; triglycerides = decreased CVD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
194
Q

What are the CV effects of rosiglitazone?

A

: LDL(not so great) and HLD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
195
Q

What are the ADRs of the TZDs?

A

Fluid retention and peripheral edema, weight gain, new onset heart failure, bone fractures, increased risk of MI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
196
Q

What are the CI of TDZs?

A

Alcohol abuse, elevated liver enzymes, hepatotoxicity, hepatic dz, and HF in class III or IV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
197
Q

What are the black box warnings for the TDZs?

A

Both: CHF
Ros: MI risk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
198
Q

What are the alpha- glucosidase inhibitors?

A

Acarbose and miglitol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
199
Q

What do the alpha-glucosidase inhibitors do?

A

Delay intestinal carb absorption

Prevents glucose absorption and decreases post-prandial glucose levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
200
Q

Is there a risk for hypoglycemia with Alpha Glucosidase inhibitors?

A

Nope

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
201
Q

What are the ADR of the alpha glucosidase inhibs?

A

Not well tolerated
GI- loose stool, flatulence, abdominal cramping
Bonus: NO WT GAIN

202
Q

How can you minimize GI effects of the alpha-gs?

A

Starting low and increase slowly

Curtailment of carb consumption

203
Q

What are the CI for alpha-gs?

A

Chronic intestinal dz and cirrhosis

204
Q

What needs to be monitored if your pt is on alpha gs?

A

Post prandial glucose at initiation and A1C in 3 months

205
Q

What are the DPP-4 inhibitors?

A

Sitagliptin, saxagliptin, algoliptin, linagliptin, and vildagliptin

206
Q

What is the MOA of the DPP-4 inhibitors?

A

Prevent the egredation of endogenous glucagon like peptide 1 and insulinotropic polypeptide
Results in increased insulin release and decreased glucagon levels in circulation in glucose dependent manner

207
Q

When does the dosage of DPP-4 inhibs need to be adjusted?

A

CrCl

208
Q

What are the ADRs of DPP-4 inhibs?

A

HA and UTI
Generally well tolerated
Investigated for pancreatic toxicity and increase in heart failure

209
Q

What should you be monitoring if your pt is on DPP-4 inhibs?

A

Renal fxn

A1C in 3 mo

210
Q

What is the bile acid sequestrant?

A

Colesevelam (welchol)

211
Q

What is the moa of colvesevelam?

A

bind bile acid in intestinal tract, increasing hepatic bile acid production- possibly decrease hepatic glucose production and increase incretin levels

212
Q

Is colvesevelam used as a monotherapy?

A

No

213
Q

What are the ADRs of colvesevelam?

A

Constipation/nausea/indigestion
triglycerides
May decrease absorption of other medications

214
Q

What are the CI of colvesevelam?

A

Bowel obstruction
History of hypertriglyceridemia-induced pancreatitis
Triglycerides >500 mg/dL

215
Q

What is the D2 agonist?

A

Bromocriptine

216
Q

What is the MOA of bromocriptine?

A

activate dopamine receptors, modulate hypothalmic regulation of metabolism, increase insulin sensitivity

217
Q

What are the benefits of bromocriptine?

A

No hypoglycemia and decreased CVD

218
Q

What are the ADRs of bromocriptine?

A

Dizzy/syncope, V, fatigue, rhinitis

219
Q

What are the SGLT2 inhibitors?

A

Canagliflozin, dapagliflozin, empagliflozin

220
Q

What is the MOA of SGLT 2 inhibs?

A

Inhibits SGLT2 in proximal nephron; Reduces reabsorption of filtered glucose thereby increasing urinary excretion of glucose

221
Q

What are the benefits of SGLT2 inhibs?

A

No hypoglycemia, decreased weight, decreased BP

222
Q

What stage of DM are SGLT2 inhibs effective at?

A

All the stages

Mono or adjunct therapy

223
Q

What are the ADRs of SGLT2 inhibs?

A

Increased potassium, renal insufficiency (with baseline GFR

224
Q

What do you need to make sure is corrected prior to initiating SGLT2 inhib tx?

A

Correct any volume depletion!

Not for pts with GFR

225
Q

What are the non oral therapies for DM II?

A

GLP-1 agonists, pramlintide or symlin, and insulin

226
Q

What are the GLP-1 agonists?

A

Exenatide, Liraglutide, Albiglutide, Lixisenatide, Dulaglutide

227
Q

What is the MOA of GLP-1 agonists?

A

Increase insulin secretion(glucose dependant), decrease glucagon secretion, slows gastric emptying, increase satiety

228
Q

What are GLP-1 agonists resistant to?

A

Degredation by DPP-4

229
Q

What is the FDA approved use for GLP-1 agonists?

A

Type 2 DM in pts on metformin, sulfonylurea, TZD, or a combo who are not at goal

230
Q

What are GLP-1 agonists NOT approved for?

A

Use with basal insulin

231
Q

What are the ADRs of GLP-1 agonists?

A
  • N/V/D (30-45%)
  • Increase Heart Rate
  • Acute Pancreatitis-possibly
  • SQ injection
  • Anti-exenatide antibodies
232
Q

What are the precautions of GLP-1s?

A

-ClCr

233
Q

What are the benefits of GLP-1?

A
  • No hypoglycemia
  • Modest weight loss
  • Decrease of some cardiovascular risk factors
234
Q

What should you monitor in a pt who is on GLP-1 tx?

A

Renal fxn and A1C in 3 mo

235
Q

What is pramlintide approved for?

A

Type I/II DM in pts on optimal insulin therapy who are still not at goal
Can be with or without metformin and or sulfon tx

236
Q

When should pramlintide be administered?

A

In conjunction with mealtime insulin

237
Q

What are the the 2 pens and their dosages for pramlintide?

A
  • SymlinPen 60: for doses of 15, 30, 45 or 60 mcg

- SymlinPen 120: for doses of 60 or 120 mcg

238
Q

If your pt has type II DM and HTN, how should you control their HTN?

A

ACEI or ARB, potential combo with a thiazide

Diet and lifestyle

239
Q

When should you screen your DM pts for dyslipidemia?

A

At DM initial evaluation and or at age 40 and q 1-2 yrs after

240
Q

What is the first choice for lowering LDL in your DM pts?

A

Statin

241
Q

When should a stain and lifestyle be added regardless of the lipid levels of your DM pt?

A
  • Overt CVD
  • Without CVD who are over the age of 40 and have one or more other CVD risk factors
  • In pts whose LDL goal can’t be achieved, a 30-40% reduction is acceptable
242
Q

If you pt has DM and CHD, how should they be tx?

A

Daily ASA unless CI

243
Q

What is hyperosmolar hyperglycemia state?

A

HHS- life threatening condition similar to DKA
Extreme hyperglycemia and fluid deficits that arises from inadequate insulin but occurs primarily in older type II DM pts

244
Q

What does HHS lack?

A

Lipolysis, ketonemia, and acidosis

245
Q

What pts are at greatest risk for developing HHS?

A

Hyperglycemia and dehydration lasting days to weeks

246
Q

What is the diagnostic criteria for HHS?

A
  • Plasma glucose > 600mg/dL

- Serum osmolality of > 320 mOsm/kg

247
Q

How is HHS tx?

A
  • Rehydration
  • Correction of electrolyte imbalances
  • Continuous insulin infusion
248
Q

What are the 3 hormones secreted by the thyroid gland?

A

T3-triiodothyronine
T4- thyroxine
Calcitonin

249
Q

What is required for hormones synthesis?

A

Iodine

250
Q

Which hormone is more potent?

A

T3

251
Q

How is t3 produced?

A

Majority is produced from the peripheral conversion of T3-T4

252
Q

What inhibits the conversion to T3?

A

BBlockers, corticosteroids, and amiodarone

253
Q

What stimulates the pituitary to syntesize and release TSH? thyrotropin-releasing hormones?

A

thyrotropin-releasing hormone TRH, from the hypothalamus

254
Q

What can block the transport of iodide into thyroid?

A

Bromide, fluoride and lithium

255
Q

What can impair the coupling of thyroid hormones?

A

Sulfonylureas and thionamides

256
Q

Thyroid hormones are released following what?

A

Proteolytic cleavage from the thyroglobulin

257
Q

What can block this release?

A

High levels of iodine or lithium

258
Q

What is free T4 level used to evaluate?

A

Free levels in euthyroid sick pts

259
Q

What does sensitive TSH valuate? When it is increased? Decreased?

A

Evaluates the pituitary negative feedback system
Increased: primary hypo
Decreased: primary hyper

260
Q

What is the definition of sub clinical hypothyroidism?

A

Serum TSH concentration above statistically defined upper limit of reference range

261
Q

What is it measured by?

A

Serum free thyroxine within reference range

262
Q

What are effects of hypothyroidism?

A 
Increased risk of CHD
—Systolic Dysfunction 
—Reduced stress tolerance during exercise
—Cardiac autonomic dysfunction
—Reduced oxygen uptake during exercise
—Diastolic hypertension
—Increased arterial stiffness
—Pro-atherosclerotic profile
—Insulin resistance
—Pro-coagulative pattern 
—Decreased activity
◦Von Willebrand factor
◦Factor VIII

increase risk for placental abruption and preterm delivery

263
Q

What are the s/s of hypothyroidism?

A 
◦Tiredness
◦Lethargy, Muscle pains
◦Weight gain
◦Intolerance to cold
◦Dry skin, Coarse skin
◦Bradycardia
◦Mental impairment
◦Dry thinning hair
264
Q

What effect does hypothyroidism have on certain drugs?

A
  • digitalis: decreases volume of distribution
  • insulin: impaired degradation
  • warfarin: delayed catabolism of clotting factors
265
Q

What are causes of primary hypothyroidism?

A

◦Hashimoto’s Disease
◦Iatrogenic hypothyroidism-radioactive iodine ingestion, post thyroidectomy
Iodine deficiency

266
Q

What are common causes of secondary hypothyroidism?

A

Pituitary dz and hypothalamic dz

267
Q

What type of pts are at increased risk for hypothyroidism?

A

◦Postpartum women
◦Family history of autoimmune thyroid disorders
◦Patients with previous head and neck of thyroid irradiation or surgery
Other autoimmune endocrine
Non-autoimmune: celiac disease, vitiligo, MS, pernicious anemia, Down’s syndrome

268
Q

What are the s/s of hypothyroidism in elderly pts?

A 
◦Hoarseness
◦Deafness
◦Confusion
◦Dementia
◦Ataxia
◦Depression
◦Dry skin
◦Hair loss
269
Q

What is the most common cause of hypothyroidism?

A

Hashimotos thyroiditis

270
Q

What is Hashimotos thyroiditis ?

A

An autoimmune disease resulting in fibrosis of the thyroid gland, antibodies to TSH receptor

271
Q

What does congenital hypothyroidism result in?

A

dwarfism and mental retardation (cretinism)

272
Q

What is myxedema?

A

When pts appear to have edema under the skin-most severe form of hypothyroidism

273
Q

What are the clinical features of myxedema?

A

◦Hypothermia
◦Advanced hypothyroid symptoms
Altered sensorium

274
Q

What can myxedema lead to?

A

Myxedema coma- high mortality rates

275
Q

What is the drug of choice for hypothyroidism management?

A

levothyroxine

276
Q

What is the MOA of levothyroxine?

A

Isomer of T4 is converted to T3

277
Q

What are the ADRs of levothyroxine?

A 
◦Arrhythmias
◦Tachycardia
◦Anginal pain
◦Cramps
◦HA
◦Restlessness
◦Sweating
◦Weight loss
◦Osteoporosis
278
Q

What is the CI for levothyroxine?

A

Thyrotoxicosis

279
Q

What how often do you need to be monitoring your pt if taking levthyroxine?

A

◦Every 6-8 weeks until TSH normalized, then every 6-12 months
◦If doses changed, recheck TSH in 2-3 months

280
Q

Levothyroxine has many drug interactions. What does it alter absorption of?

A

◦Cholestyramine
◦Ferrous sulfate
◦Sucralfate
Aluminum hydroxide

281
Q

Levothyroxine has many drug interactions. What does it incease the metabolism of?

A

◦Rifampin
◦Phenytoin
◦Carbamazepine

282
Q

What is the effect of oral contraceptives or estrogen with levo?

A

◦Increase thyroid binding globulin, resulting in lower free thyroid hormone

283
Q

What is the effect of lithium with levo?

A

◦Inhibits synthesis and release of thyroid hormone

284
Q

What is the effect of amiodarone with levo?

A

Block conversion T4 to T3

285
Q

What is the effect of warfarin with levo?

A

Increases metabolism of clotting factors

286
Q

What are the other 2 drug choices for hypothyroidism management?

A

Liothyronine sodium and liotrix

287
Q

Why is liothyronine generally not used for maintenance?

A

therapy because of its short half-life and duration of action.

288
Q

What are the indications for liothyronine?

A

–Initial therapy of myxedema (skin disorder) and myxedema coma
–Short-term suppression of TSH in patients undergoing surgery for thyroid cancer.
–Patients w/5’-deiodinase deficiency who cannot convert T4 to T3.

289
Q

Is liotrix any more effective than levo?

A

No

290
Q

What is the specific tx regime for myxedema coma?

A

◦IV bolus levothyroxine 300-500mcg
◦Maintenance 75-100 mcg IV until able to switch to PO
◦IV hydrocortisone 100mg q 8h until coexisting adrenal suppression is ruled out
◦Supportive therapy- ventillation, euglycemia, blood pressure, body temp maintained

291
Q

What is the specific tx for congenital hypothyroidism?

A

◦Initial therapy within 45 days of birth at 10-15mcg/kg/d, associated with improved IQ’s in treated infants
◦Dose progressively decreased to typical adult dose beginning 11-20 years
- aggressive tx important for normal development!

292
Q

How is hypothyroidism tx in pregnancy?

A

—Treatment: levothyroxine
◦20% requires dose increase during pregnancy/ decrease after
◦Typically require 36 mcg/day increase in dosage

293
Q

What causes hyperthyroidism?

A

◦Overproduction of endogenous hormone
◦Exposure to excess endogenous hormone
◦Elevated free and total T3, T4 or both serum concentrations

294
Q

What are the subclinical and clinical serum levels of TSH for diagnosis?

A

—Subclinical

◦TSH 13.2 mcg/dL

295
Q

What are S/S of hyperthyroidism?

A 
◦Nervousness
◦Anxiety
◦Palpitations
◦Increased basal metabolic rate (BMR)
◦Weight loss
◦Increased appetite
◦Increased body temp (heat intolerance)
◦Sweating
◦Fine Tremor
◦Tachycardia
◦Classical ophthalmic signs
296
Q

What is the most common cause of hyperthyroidism?

A

Graves dz

297
Q

What is graves dz?

A

Autoimmune syndrome that includes hyperthyroidism, diffuse thyroid enlargement, myxedema, thyroid acropachy

298
Q

What forms against the thyroid cell?

A

IgG antibodies bind and activate the receptor

299
Q

Why is TSH undetectable in graves?

A

From the negative feedback from elevated thyroid hormone- disproportionate increase in T3 compared to T4

300
Q

What is the most common cause of hyperthyroidism in preggo?

A

Graves

Inappropriate production of hCG can cause subclinical or overt hyperthyroidism

301
Q

What are common complications if hyperthyroidism is left untreated in the preggos?

A

◦Spontaneous abortion
◦Premature delivery
◦Low birth weight
◦Eclampsia

302
Q

What is the drug of choice for tx graves in preggo?

A

PTU at the lowest effective dose

303
Q

What is a thyroid storm?

A

Life threatening medical emergency characterized by ◦Severe thyrotoxicosis, high fever (often > 103 F), tachycardia, tachypnea, dehydration, delirium-coma, N/V, and diarrhea

304
Q

What are the precipitating factors to a thyroid storm?

A

◦Infection, trauma, surgery radioactive iodine treatment, withdrawl from antithyroid drugs

305
Q

How can you tx a thyroid storm?

A

◦Suppression of thyroid hormone formation and secretion
◦Anti-adrenergic therapy
◦Administration corticosteroids
◦Treatment of complications

306
Q

What are the pharmacologic options for hyperthyroidism?

A

Thioamides, Iodines and iodine containing agents. Radioiodine, Lithium carbonate, Beta adrenergic antagonists, corticosteroids

307
Q

What are the thioamides?

A

PTU- propylthiouracil

MMI- methimazole

308
Q

What is the MOA of the thioamides?

A

Block thyroid hormone synthesis

PTU also inhibits DI which deiodinates peripheral T4 to T3

309
Q

What are the indications for the thioamides?

A

◦Management of hyperthyroidism
◦Thyrotoxic crisis
◦In the preparation of patients for surgical subtotal thyroidectomy

310
Q

Why might MMI be preferred?

A

Generally has fewer side effect and is 10x more potent than PTU, meaning it requires lower dosages

311
Q

What are the most frequent ADRs of thioamides?

A 
–Rash
–Arthralgia
–Myalgia
–Cholestatic jaundice
–Lymphadenopathy
–Drug fever
–Psychosis
–Alopecia
312
Q

What are the most serious ADRs of the thioamides? When do they typically happen?

A

Within first 3 mo of therapy
–Arganulocytosis-must obtain baseline white blood cell count (stop if develop fever or sore throat)
–Hepatotoxicity-baseline white blood cell count (stop if pt. develops fever or sore throat)
–Vasculitis-drug induced lupus or anti-neutrophil

313
Q

What can thioamides cause in excessive amounts over long periods of time?

A

Hypothyroidism and enlargement of the thyroid gland

314
Q

What are indications for the iodines and iodine containing agents?

A

◦Preoperatively for thyroidectomy (7-14 days)

◦Used after RAI (3-7 days), to allow RAI to concentrate in thyroid

315
Q

What are the CI for iodines?

A

Should not be given to breastfeeding women- can cause goiter in infants

316
Q

How are the iodines administered?

A

Iodine and iodide are given 10-14 days prior to partial thyroidectomy w/PTU or methimazole

317
Q

Should you give iodines long term?

A

No- they loose effectiveness

318
Q

What are the ADRs of the iodines?

A 
◦Hypersensitivity rxn
◦HA
◦Lacrimation
◦Conjunctivitis
◦Laryngitis
◦Thyrotoxicosis in patients w/nontoxic goiter
◦Drug fever
◦Acneform rash
◦Metallic taste in mouth
319
Q

When is radioiodine used?

A

For thyroid ablation in the management of hyperthyroidism

320
Q

When is radioiodine the agent of choice?

A

Graves, toxic autonomous nodules, toxic multinodular goiters

321
Q

What is the goal of radioiodine? MOA?

A

To destroy overactive thyroid cells
◦Taken up by other organs- organification only in thyroid
◦The ablative effect is exerted primarily through beta-particle emissions, which destroy thyroid tissue.

322
Q

What is the major disadvantage to using radioiodine?

A

◦Hypothyroidism in most patients
◦Can not be used in pregnancy
◦Hypothyroid often occurs months-years after RAI
◦African Americans are most likely to be resistant to RAI (require multiple doses)

323
Q

What is the MOA of lithium carbonate?

A

◦Lithium inhibits thyroidal incorporation of I- into thyroid gland which inhibits the secretion of thyroid hormones from follicular cells

324
Q

What are the indications for lithium carbonate?

A

Offers no advantage over thioamide

Can be used for temporary control of thyrotoxicosis in pts allergic to thioamides and iodine

325
Q

When are beta-adrenergic antagonists used in hyperthyroidism?

A

to ameliorate thyrotoxic symptoms: palpitations, anxiety, tremor, heat intolerance

326
Q

Is it a primary or adjunct therapy?

A

Adjunct! No effect on peripheral thyrotixicosis and therapeutic effect

327
Q

Which corticosteroids can be used in hyperthyroidism?

A

—Dexamethasone
—Prednisone
—Methylprednisolone
—Hyrocortisone

328
Q

What are the effects of the corticosteroids?

A

◦Decreases thyroid action
◦Decreases immune response in Grave’s disease
reduce T3

329
Q

When are corticosteroids useful?

A

Thyroiditis and thyroid storm

330
Q

When is a thyroidectomy indicated?

A

large glands, severe ophthalmopathy, lack of remission on treatment

331
Q

What pts should not have a thyroidectomy?

A

On pts with low RAI uptake

332
Q

What medications should the pt be on before during and after the surgery?

A

—Propylthiouracil (PTU) or methimazole (MMI) until pt is euthyroid (6-8 weeks) followed by iodide 500 mg/day x 10-14 days
—Beta blocker (propranolol/ nadolol) pre- and post-surgery to maintain HR

333
Q

What are complications of a thyroidectomy?

A

◦Hyperthyroidism
◦Hypothyroidism
◦Hypoparathyroidism
◦Vocal cord abnormalities

334
Q

What are drugs your pt may be taking that if you added a thyroid or antithyroid agent would have interactions?

A

◦Warfarin
◦Lithium
◦Diabetes medication requirements may change
◦Potassium iodide used as expectorants
◦Cardiac glycosides such as digoxin may require dosage adjustments
◦Amiodarone
CNS depressants

335
Q

Amiodarone and iodinated contrast media can inhibit conversion of T4 to T3 in peripheral circulation and the pituitary gland. What are the levels and when do these happen?

A

–Iodinated Contrast
‭ ‬Reduction in levels in week 1
‭ ‬Return to normal by week 2
–Amiodarone
‭ ‬Transient elevation in TSH during first 3 months
‭ ‬Persistent FT4 elevations and reduced T3 in on-going therapy

336
Q

What prescription drugs containing iodides can induce thyroid dz?

A

–Amiodarone
–Radiocontrast dye
–Povidone iodine
–Iodinated glycerol

337
Q

What non-prescription drugs containing iodides can induce thyroid dz?

A

–Cough and cold
–Kelp
–Herbals
–Dietary supplements/ weight loss products

338
Q

What is iodine induced hyperthyroidism called?

A

Jod-basedow dz

339
Q

When does jod-b develop and how is it tx?

A

◦Develops within 3-8 weeks after exposure in up to 5% pts

◦Treatment with thioamides and beta blockers

340
Q

What pts are at risk of developing iodine induced hypothyroidism?

A

Pts being tx with Amiodarone

341
Q

How is iodine induced hypothyroidism tx?

A

levothyroxine replacement

342
Q

What other drug can induce hypothyroidism? How is this tx?

A

Lithium- more like if tx >2ys
Tx: levo to reverse
◦Can spontaneously resolve without treatment
◦Stopping lithium does not always resolve symptoms or goiter
◦May require surgical intervention

343
Q

When might interferon alpha induced thyroid dz present?

A

within 6-8 weeks of starting therapy or occur 6-23 months after start

344
Q

How is IFNa induced dz tx?

A

Hypothyroidism resolves spontaneously within 2-3 months after stopping therapy in most patients- may take longer

345
Q

What are the 3 hormones secreted by the thyroid gland?

A

T3-triiodothyronine
T4- thyroxine
Calcitonin

346
Q

What is required for hormones synthesis?

A

Iodine

347
Q

Which hormone is more potent?

A

T3

348
Q

How is t3 produced?

A

Majority is produced from the peripheral conversion of T3-T4

349
Q

What inhibits the conversion to T3?

A

BBlockers, corticosteroids, and amiodarone

350
Q

What stimulates the pituitary to syntesize and release TSH? thyrotropin-releasing hormones?

A

thyrotropin-releasing hormone TRH, from the hypothalamus

351
Q

What can block the transport of iodide into thyroid?

A

Bromide, fluoride and lithium

352
Q

What can impair the coupling of thyroid hormones?

A

Sulfonylureas and thionamides

353
Q

Thyroid hormones are released following what?

A

Proteolytic cleavage from the thyroglobulin

354
Q

What can block this release?

A

High levels of iodine or lithium

355
Q

What is free T4 level used to evaluate?

A

Free levels in euthyroid sick pts

356
Q

What does sensitive TSH valuate? When it is increased? Decreased?

A

Evaluates the pituitary negative feedback system
Increased: primary hypo
Decreased: primary hyper

357
Q

What is the definition of sub clinical hypothyroidism?

A

Serum TSH concentration above statistically defined upper limit of reference range

358
Q

What is it measured by?

A

Serum free thyroxine within reference range

359
Q

What are effects of hypothyroidism?

A 
Increased risk of CHD
—Systolic Dysfunction 
—Reduced stress tolerance during exercise
—Cardiac autonomic dysfunction
—Reduced oxygen uptake during exercise
—Diastolic hypertension
—Increased arterial stiffness
—Pro-atherosclerotic profile
—Insulin resistance
—Pro-coagulative pattern 
—Decreased activity
◦Von Willebrand factor
◦Factor VIII

increase risk for placental abruption and preterm delivery

360
Q

What are the s/s of hypothyroidism?

A 
◦Tiredness
◦Lethargy, Muscle pains
◦Weight gain
◦Intolerance to cold
◦Dry skin, Coarse skin
◦Bradycardia
◦Mental impairment
◦Dry thinning hair
361
Q

What effect does hypothyroidism have on certain drugs?

A
  • digitalis: decreases volume of distribution
  • insulin: impaired degradation
  • warfarin: delayed catabolism of clotting factors
362
Q

What are causes of primary hypothyroidism?

A

◦Hashimoto’s Disease
◦Iatrogenic hypothyroidism-radioactive iodine ingestion, post thyroidectomy
Iodine deficiency

363
Q

What are common causes of secondary hypothyroidism?

A

Pituitary dz and hypothalamic dz

364
Q

What type of pts are at increased risk for hypothyroidism?

A

◦Postpartum women
◦Family history of autoimmune thyroid disorders
◦Patients with previous head and neck of thyroid irradiation or surgery
Other autoimmune endocrine
Non-autoimmune: celiac disease, vitiligo, MS, pernicious anemia, Down’s syndrome

365
Q

What are the s/s of hypothyroidism in elderly pts?

A 
◦Hoarseness
◦Deafness
◦Confusion
◦Dementia
◦Ataxia
◦Depression
◦Dry skin
◦Hair loss
366
Q

What is the most common cause of hypothyroidism?

A

Hashimotos thyroiditis

367
Q

What is Hashimotos thyroiditis ?

A

An autoimmune disease resulting in fibrosis of the thyroid gland, antibodies to TSH receptor

368
Q

What does congenital hypothyroidism result in?

A

dwarfism and mental retardation (cretinism)

369
Q

What is myxedema?

A

When pts appear to have edema under the skin-most severe form of hypothyroidism

370
Q

What are the clinical features of myxedema?

A

◦Hypothermia
◦Advanced hypothyroid symptoms
Altered sensorium

371
Q

What can myxedema lead to?

A

Myxedema coma- high mortality rates

372
Q

What is the drug of choice for hypothyroidism management?

A

levothyroxine

373
Q

What is the MOA of levothyroxine?

A

Isomer of T4 is converted to T3

374
Q

What are the ADRs of levothyroxine?

A 
◦Arrhythmias
◦Tachycardia
◦Anginal pain
◦Cramps
◦HA
◦Restlessness
◦Sweating
◦Weight loss
◦Osteoporosis
375
Q

What is the CI for levothyroxine?

A

Thyrotoxicosis

376
Q

What how often do you need to be monitoring your pt if taking levthyroxine?

A

◦Every 6-8 weeks until TSH normalized, then every 6-12 months
◦If doses changed, recheck TSH in 2-3 months

377
Q

Levothyroxine has many drug interactions. What does it alter absorption of?

A

◦Cholestyramine
◦Ferrous sulfate
◦Sucralfate
Aluminum hydroxide

378
Q

Levothyroxine has many drug interactions. What does it incease the metabolism of?

A

◦Rifampin
◦Phenytoin
◦Carbamazepine

379
Q

What is the effect of oral contraceptives or estrogen with levo?

A

◦Increase thyroid binding globulin, resulting in lower free thyroid hormone

380
Q

What is the effect of lithium with levo?

A

◦Inhibits synthesis and release of thyroid hormone

381
Q

What is the effect of amiodarone with levo?

A

Block conversion T4 to T3

382
Q

What is the effect of warfarin with levo?

A

Increases metabolism of clotting factors

383
Q

What are the other 2 drug choices for hypothyroidism management?

A

Liothyronine sodium and liotrix

384
Q

Why is liothyronine generally not used for maintenance?

A

therapy because of its short half-life and duration of action.

385
Q

What are the indications for liothyronine?

A

–Initial therapy of myxedema (skin disorder) and myxedema coma
–Short-term suppression of TSH in patients undergoing surgery for thyroid cancer.
–Patients w/5’-deiodinase deficiency who cannot convert T4 to T3.

386
Q

Is liotrix any more effective than levo?

A

No

387
Q

What is the specific tx regime for myxedema coma?

A

◦IV bolus levothyroxine 300-500mcg
◦Maintenance 75-100 mcg IV until able to switch to PO
◦IV hydrocortisone 100mg q 8h until coexisting adrenal suppression is ruled out
◦Supportive therapy- ventillation, euglycemia, blood pressure, body temp maintained

388
Q

What is the specific tx for congenital hypothyroidism?

A

◦Initial therapy within 45 days of birth at 10-15mcg/kg/d, associated with improved IQ’s in treated infants
◦Dose progressively decreased to typical adult dose beginning 11-20 years
- aggressive tx important for normal development!

389
Q

How is hypothyroidism tx in pregnancy?

A

—Treatment: levothyroxine
◦20% requires dose increase during pregnancy/ decrease after
◦Typically require 36 mcg/day increase in dosage

390
Q

What causes hyperthyroidism?

A

◦Overproduction of endogenous hormone
◦Exposure to excess endogenous hormone
◦Elevated free and total T3, T4 or both serum concentrations

391
Q

What are the subclinical and clinical serum levels of TSH for diagnosis?

A

—Subclinical

◦TSH 13.2 mcg/dL

392
Q

What are S/S of hyperthyroidism?

A 
◦Nervousness
◦Anxiety
◦Palpitations
◦Increased basal metabolic rate (BMR)
◦Weight loss
◦Increased appetite
◦Increased body temp (heat intolerance)
◦Sweating
◦Fine Tremor
◦Tachycardia
◦Classical ophthalmic signs
393
Q

What is the most common cause of hyperthyroidism?

A

Graves dz

394
Q

What is graves dz?

A

Autoimmune syndrome that includes hyperthyroidism, diffuse thyroid enlargement, myxedema, thyroid acropachy

395
Q

What forms against the thyroid cell?

A

IgG antibodies bind and activate the receptor

396
Q

Why is TSH undetectable in graves?

A

From the negative feedback from elevated thyroid hormone- disproportionate increase in T3 compared to T4

397
Q

What is the most common cause of hyperthyroidism in preggo?

A

Graves

Inappropriate production of hCG can cause subclinical or overt hyperthyroidism

398
Q

What are common complications if hyperthyroidism is left untreated in the preggos?

A

◦Spontaneous abortion
◦Premature delivery
◦Low birth weight
◦Eclampsia

399
Q

What is the drug of choice for tx graves in preggo?

A

PTU at the lowest effective dose

400
Q

What is a thyroid storm?

A

Life threatening medical emergency characterized by ◦Severe thyrotoxicosis, high fever (often > 103 F), tachycardia, tachypnea, dehydration, delirium-coma, N/V, and diarrhea

401
Q

What are the precipitating factors to a thyroid storm?

A

◦Infection, trauma, surgery radioactive iodine treatment, withdrawl from antithyroid drugs

402
Q

How can you tx a thyroid storm?

A

◦Suppression of thyroid hormone formation and secretion
◦Anti-adrenergic therapy
◦Administration corticosteroids
◦Treatment of complications

403
Q

What are the pharmacologic options for hyperthyroidism?

A

Thioamides, Iodines and iodine containing agents. Radioiodine, Lithium carbonate, Beta adrenergic antagonists, corticosteroids

404
Q

What are the thioamides?

A

PTU- propylthiouracil

MMI- methimazole

405
Q

What is the MOA of the thioamides?

A

Block thyroid hormone synthesis

PTU also inhibits DI which deiodinates peripheral T4 to T3

406
Q

What are the indications for the thioamides?

A

◦Management of hyperthyroidism
◦Thyrotoxic crisis
◦In the preparation of patients for surgical subtotal thyroidectomy

407
Q

Why might MMI be preferred?

A

Generally has fewer side effect and is 10x more potent than PTU, meaning it requires lower dosages

408
Q

What are the most frequent ADRs of thioamides?

A 
–Rash
–Arthralgia
–Myalgia
–Cholestatic jaundice
–Lymphadenopathy
–Drug fever
–Psychosis
–Alopecia
409
Q

What are the most serious ADRs of the thioamides? When do they typically happen?

A

Within first 3 mo of therapy
–Arganulocytosis-must obtain baseline white blood cell count (stop if develop fever or sore throat)
–Hepatotoxicity-baseline white blood cell count (stop if pt. develops fever or sore throat)
–Vasculitis-drug induced lupus or anti-neutrophil

410
Q

What can thioamides cause in excessive amounts over long periods of time?

A

Hypothyroidism and enlargement of the thyroid gland

411
Q

What are indications for the iodines and iodine containing agents?

A

◦Preoperatively for thyroidectomy (7-14 days)

◦Used after RAI (3-7 days), to allow RAI to concentrate in thyroid

412
Q

What are the CI for iodines?

A

Should not be given to breastfeeding women- can cause goiter in infants

413
Q

How are the iodines administered?

A

Iodine and iodide are given 10-14 days prior to partial thyroidectomy w/PTU or methimazole

414
Q

Should you give iodines long term?

A

No- they loose effectiveness

415
Q

What are the ADRs of the iodines?

A 
◦Hypersensitivity rxn
◦HA
◦Lacrimation
◦Conjunctivitis
◦Laryngitis
◦Thyrotoxicosis in patients w/nontoxic goiter
◦Drug fever
◦Acneform rash
◦Metallic taste in mouth
416
Q

When is radioiodine used?

A

For thyroid ablation in the management of hyperthyroidism

417
Q

When is radioiodine the agent of choice?

A

Graves, toxic autonomous nodules, toxic multinodular goiters

418
Q

What is the goal of radioiodine? MOA?

A

To destroy overactive thyroid cells
◦Taken up by other organs- organification only in thyroid
◦The ablative effect is exerted primarily through beta-particle emissions, which destroy thyroid tissue.

419
Q

What is the major disadvantage to using radioiodine?

A

◦Hypothyroidism in most patients
◦Can not be used in pregnancy
◦Hypothyroid often occurs months-years after RAI
◦African Americans are most likely to be resistant to RAI (require multiple doses)

420
Q

What is the MOA of lithium carbonate?

A

◦Lithium inhibits thyroidal incorporation of I- into thyroid gland which inhibits the secretion of thyroid hormones from follicular cells

421
Q

What are the indications for lithium carbonate?

A

Offers no advantage over thioamide

Can be used for temporary control of thyrotoxicosis in pts allergic to thioamides and iodine

422
Q

When are beta-adrenergic antagonists used in hyperthyroidism?

A

to ameliorate thyrotoxic symptoms: palpitations, anxiety, tremor, heat intolerance

423
Q

Is it a primary or adjunct therapy?

A

Adjunct! No effect on peripheral thyrotixicosis and therapeutic effect

424
Q

Which corticosteroids can be used in hyperthyroidism?

A

—Dexamethasone
—Prednisone
—Methylprednisolone
—Hyrocortisone

425
Q

What are the effects of the corticosteroids?

A

◦Decreases thyroid action
◦Decreases immune response in Grave’s disease
reduce T3

426
Q

When are corticosteroids useful?

A

Thyroiditis and thyroid storm

427
Q

When is a thyroidectomy indicated?

A

large glands, severe ophthalmopathy, lack of remission on treatment

428
Q

What pts should not have a thyroidectomy?

A

On pts with low RAI uptake

429
Q

What medications should the pt be on before during and after the surgery?

A

—Propylthiouracil (PTU) or methimazole (MMI) until pt is euthyroid (6-8 weeks) followed by iodide 500 mg/day x 10-14 days
—Beta blocker (propranolol/ nadolol) pre- and post-surgery to maintain HR

430
Q

What are complications of a thyroidectomy?

A

◦Hyperthyroidism
◦Hypothyroidism
◦Hypoparathyroidism
◦Vocal cord abnormalities

431
Q

What are drugs your pt may be taking that if you added a thyroid or antithyroid agent would have interactions?

A

◦Warfarin
◦Lithium
◦Diabetes medication requirements may change
◦Potassium iodide used as expectorants
◦Cardiac glycosides such as digoxin may require dosage adjustments
◦Amiodarone
CNS depressants

432
Q

Amiodarone and iodinated contrast media can inhibit conversion of T4 to T3 in peripheral circulation and the pituitary gland. What are the levels and when do these happen?

A

–Iodinated Contrast
‭ ‬Reduction in levels in week 1
‭ ‬Return to normal by week 2
–Amiodarone
‭ ‬Transient elevation in TSH during first 3 months
‭ ‬Persistent FT4 elevations and reduced T3 in on-going therapy

433
Q

What prescription drugs containing iodides can induce thyroid dz?

A

–Amiodarone
–Radiocontrast dye
–Povidone iodine
–Iodinated glycerol

434
Q

What non-prescription drugs containing iodides can induce thyroid dz?

A

–Cough and cold
–Kelp
–Herbals
–Dietary supplements/ weight loss products

435
Q

What is iodine induced hyperthyroidism called?

A

Jod-basedow dz

436
Q

When does jod-b develop and how is it tx?

A

◦Develops within 3-8 weeks after exposure in up to 5% pts

◦Treatment with thioamides and beta blockers

437
Q

What pts are at risk of developing iodine induced hypothyroidism?

A

Pts being tx with Amiodarone

438
Q

How is iodine induced hypothyroidism tx?

A

levothyroxine replacement

439
Q

What other drug can induce hypothyroidism? How is this tx?

A

Lithium- more like if tx >2ys
Tx: levo to reverse
◦Can spontaneously resolve without treatment
◦Stopping lithium does not always resolve symptoms or goiter
◦May require surgical intervention

440
Q

When might interferon alpha induced thyroid dz present?

A

within 6-8 weeks of starting therapy or occur 6-23 months after start

441
Q

How is IFNa induced dz tx?

A

Hypothyroidism resolves spontaneously within 2-3 months after stopping therapy in most patients- may take longer

442
Q

What are the precipitating factors to a thyroid storm?

A

◦Infection, trauma, surgery radioactive iodine treatment, withdrawl from antithyroid drugs

443
Q

How can you tx a thyroid storm?

A

◦Suppression of thyroid hormone formation and secretion
◦Anti-adrenergic therapy
◦Administration corticosteroids
◦Treatment of complications

444
Q

What are the pharmacologic options for hyperthyroidism?

A

Thioamides, Iodines and iodine containing agents. Radioiodine, Lithium carbonate, Beta adrenergic antagonists, corticosteroids

445
Q

What are the thioamides?

A

PTU- propylthiouracil

MMI- methimazole

446
Q

What is the MOA of the thioamides?

A

Block thyroid hormone synthesis

PTU also inhibits DI which deiodinates peripheral T4 to T3

447
Q

What are the indications for the thioamides?

A

◦Management of hyperthyroidism
◦Thyrotoxic crisis
◦In the preparation of patients for surgical subtotal thyroidectomy

448
Q

Why might MMI be preferred?

A

Generally has fewer side effect and is 10x more potent than PTU, meaning it requires lower dosages

449
Q

What are the most frequent ADRs of thioamides?

A 
–Rash
–Arthralgia
–Myalgia
–Cholestatic jaundice
–Lymphadenopathy
–Drug fever
–Psychosis
–Alopecia
450
Q

What are the most serious ADRs of the thioamides? When do they typically happen?

A

Within first 3 mo of therapy
–Arganulocytosis-must obtain baseline white blood cell count (stop if develop fever or sore throat)
–Hepatotoxicity-baseline white blood cell count (stop if pt. develops fever or sore throat)
–Vasculitis-drug induced lupus or anti-neutrophil

451
Q

What can thioamides cause in excessive amounts over long periods of time?

A

Hypothyroidism and enlargement of the thyroid gland

452
Q

What are indications for the iodines and iodine containing agents?

A

◦Preoperatively for thyroidectomy (7-14 days)

◦Used after RAI (3-7 days), to allow RAI to concentrate in thyroid

453
Q

What are the CI for iodines?

A

Should not be given to breastfeeding women- can cause goiter in infants

454
Q

How are the iodines administered?

A

Iodine and iodide are given 10-14 days prior to partial thyroidectomy w/PTU or methimazole

455
Q

Should you give iodines long term?

A

No- they loose effectiveness

456
Q

What are the ADRs of the iodines?

A 
◦Hypersensitivity rxn
◦HA
◦Lacrimation
◦Conjunctivitis
◦Laryngitis
◦Thyrotoxicosis in patients w/nontoxic goiter
◦Drug fever
◦Acneform rash
◦Metallic taste in mouth
457
Q

When is radioiodine used?

A

For thyroid ablation in the management of hyperthyroidism

458
Q

When is radioiodine the agent of choice?

A

Graves, toxic autonomous nodules, toxic multinodular goiters

459
Q

What is the goal of radioiodine? MOA?

A

To destroy overactive thyroid cells
◦Taken up by other organs- organification only in thyroid
◦The ablative effect is exerted primarily through beta-particle emissions, which destroy thyroid tissue.

460
Q

What is the major disadvantage to using radioiodine?

A

◦Hypothyroidism in most patients
◦Can not be used in pregnancy
◦Hypothyroid often occurs months-years after RAI
◦African Americans are most likely to be resistant to RAI (require multiple doses)

461
Q

What is the MOA of lithium carbonate?

A

◦Lithium inhibits thyroidal incorporation of I- into thyroid gland which inhibits the secretion of thyroid hormones from follicular cells

462
Q

What are the indications for lithium carbonate?

A

Offers no advantage over thioamide

Can be used for temporary control of thyrotoxicosis in pts allergic to thioamides and iodine

463
Q

When are beta-adrenergic antagonists used in hyperthyroidism?

A

to ameliorate thyrotoxic symptoms: palpitations, anxiety, tremor, heat intolerance

464
Q

Is it a primary or adjunct therapy?

A

Adjunct! No effect on peripheral thyrotixicosis and therapeutic effect

465
Q

Which corticosteroids can be used in hyperthyroidism?

A

—Dexamethasone
—Prednisone
—Methylprednisolone
—Hyrocortisone

466
Q

What are the effects of the corticosteroids?

A

◦Decreases thyroid action
◦Decreases immune response in Grave’s disease
reduce T3

467
Q

When are corticosteroids useful?

A

Thyroiditis and thyroid storm

468
Q

When is a thyroidectomy indicated?

A

large glands, severe ophthalmopathy, lack of remission on treatment

469
Q

What pts should not have a thyroidectomy?

A

On pts with low RAI uptake

470
Q

What medications should the pt be on before during and after the surgery?

A

—Propylthiouracil (PTU) or methimazole (MMI) until pt is euthyroid (6-8 weeks) followed by iodide 500 mg/day x 10-14 days
—Beta blocker (propranolol/ nadolol) pre- and post-surgery to maintain HR

471
Q

What are complications of a thyroidectomy?

A

◦Hyperthyroidism
◦Hypothyroidism
◦Hypoparathyroidism
◦Vocal cord abnormalities

472
Q

What are drugs your pt may be taking that if you added a thyroid or antithyroid agent would have interactions?

A

◦Warfarin
◦Lithium
◦Diabetes medication requirements may change
◦Potassium iodide used as expectorants
◦Cardiac glycosides such as digoxin may require dosage adjustments
◦Amiodarone
CNS depressants

473
Q

Amiodarone and iodinated contrast media can inhibit conversion of T4 to T3 in peripheral circulation and the pituitary gland. What are the levels and when do these happen?

A

–Iodinated Contrast
‭ ‬Reduction in levels in week 1
‭ ‬Return to normal by week 2
–Amiodarone
‭ ‬Transient elevation in TSH during first 3 months
‭ ‬Persistent FT4 elevations and reduced T3 in on-going therapy

474
Q

What prescription drugs containing iodides can induce thyroid dz?

A

–Amiodarone
–Radiocontrast dye
–Povidone iodine
–Iodinated glycerol

475
Q

What non-prescription drugs containing iodides can induce thyroid dz?

A

–Cough and cold
–Kelp
–Herbals
–Dietary supplements/ weight loss products

476
Q

What is iodine induced hyperthyroidism called?

A

Jod-basedow dz

477
Q

When does jod-b develop and how is it tx?

A

◦Develops within 3-8 weeks after exposure in up to 5% pts

◦Treatment with thioamides and beta blockers

478
Q

What pts are at risk of developing iodine induced hypothyroidism?

A

Pts being tx with Amiodarone

479
Q

How is iodine induced hypothyroidism tx?

A

levothyroxine replacement

480
Q

What other drug can induce hypothyroidism? How is this tx?

A

Lithium- more like if tx >2ys
Tx: levo to reverse
◦Can spontaneously resolve without treatment
◦Stopping lithium does not always resolve symptoms or goiter
◦May require surgical intervention

481
Q

When might interferon alpha induced thyroid dz present?

A

within 6-8 weeks of starting therapy or occur 6-23 months after start

482
Q

How is IFNa induced dz tx?

A

Hypothyroidism resolves spontaneously within 2-3 months after stopping therapy in most patients- may take longer

483
Q

What are indications for the iodines and iodine containing agents?

A

◦Preoperatively for thyroidectomy (7-14 days)

◦Used after RAI (3-7 days), to allow RAI to concentrate in thyroid

484
Q

What are the CI for iodines?

A

Should not be given to breastfeeding women- can cause goiter in infants

485
Q

How are the iodines administered?

A

Iodine and iodide are given 10-14 days prior to partial thyroidectomy w/PTU or methimazole

486
Q

Should you give iodines long term?

A

No- they loose effectiveness

487
Q

What are the ADRs of the iodines?

A 
◦Hypersensitivity rxn
◦HA
◦Lacrimation
◦Conjunctivitis
◦Laryngitis
◦Thyrotoxicosis in patients w/nontoxic goiter
◦Drug fever
◦Acneform rash
◦Metallic taste in mouth
488
Q

When is radioiodine used?

A

For thyroid ablation in the management of hyperthyroidism

489
Q

When is radioiodine the agent of choice?

A

Graves, toxic autonomous nodules, toxic multinodular goiters

490
Q

What is the goal of radioiodine? MOA?

A

To destroy overactive thyroid cells
◦Taken up by other organs- organification only in thyroid
◦The ablative effect is exerted primarily through beta-particle emissions, which destroy thyroid tissue.

491
Q

What is the major disadvantage to using radioiodine?

A

◦Hypothyroidism in most patients
◦Can not be used in pregnancy
◦Hypothyroid often occurs months-years after RAI
◦African Americans are most likely to be resistant to RAI (require multiple doses)

492
Q

What is the MOA of lithium carbonate?

A

◦Lithium inhibits thyroidal incorporation of I- into thyroid gland which inhibits the secretion of thyroid hormones from follicular cells

493
Q

What are the indications for lithium carbonate?

A

Offers no advantage over thioamide

Can be used for temporary control of thyrotoxicosis in pts allergic to thioamides and iodine

494
Q

When are beta-adrenergic antagonists used in hyperthyroidism?

A

to ameliorate thyrotoxic symptoms: palpitations, anxiety, tremor, heat intolerance

495
Q

Is it a primary or adjunct therapy?

A

Adjunct! No effect on peripheral thyrotixicosis and therapeutic effect

496
Q

Which corticosteroids can be used in hyperthyroidism?

A

—Dexamethasone
—Prednisone
—Methylprednisolone
—Hyrocortisone

497
Q

What are the effects of the corticosteroids?

A

◦Decreases thyroid action
◦Decreases immune response in Grave’s disease
reduce T3

498
Q

When are corticosteroids useful?

A

Thyroiditis and thyroid storm

499
Q

When is a thyroidectomy indicated?

A

large glands, severe ophthalmopathy, lack of remission on treatment

500
Q

What pts should not have a thyroidectomy?

A

On pts with low RAI uptake

DOOS 2 (14 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions