Brainscape's Knowledge GenomeTM

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


See full index

Endocrinology > Diabetes > Flashcards

Diabetes Flashcards

1
Q

What is the appropriate screening for DM in a patient with HIV infection?

A

Measure fasting glucose every 3 months after starting or changing antiretroviral therapy.
Increased risk for DM d/t insulin resistance and maybe beta cell death.

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

Diabetic amyotrophy:

  1. treatment?
  2. etiology?
A
  1. symptomatic management only: tricyclic antidepressants (“-iptylines and amines”), “gaba’s” (pregabalin and gabapentin), and duloxetine (SNRI). Duloxetine is FDA approved for painful diabetic neuropathy
  2. ischemia due to microscopic polyangiitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

MODY 3:

  1. Due to what mutation? MOA
  2. Prevalence
  3. Treatment
A
  1. HNF1A.
    MOA - abnormal insulin secretion, low renal threshold for glucose; therefore +glucosuria
  2. Most common
  3. sulfonylurea
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

MODY 2

  1. Due to what mutation?
  2. Prevalence
  3. Treatment
A
  1. GCK gene.
    MOA- defective glucokinase molecule (glucose sensor), increased plasma levels of glucose are needed to elicit normal levels of insulin secretion
  2. 15-30% of MODY
    3.** Diet**. Patients do **not **typically develop microangiopathic complications.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

MODY 1

  1. Due to what mutation?
  2. Prevalence
  3. Treatment
A

1.HNF4A
MOA-reduced insulin secretory response to glucose; no glucosuria
2. 3rd most common MODY
3. SU

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

Black patients are more likely to respond to what BP meds?

A

diuretics (chlorthalidone) and calcium-channel blockers than to ACEIs. They are also more likely to require more than 1 agent for HTN control

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

What are the key results of the CONCEPTT trial regarding glycemic control in pregnant patients?

A

pregnant patients with T1DM in the CGM group had significant improvements in glycemic control at 34 weeks’ gestation vs POC checks. The risk of neonatal complications was much reduced.

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

Drugs that can cause a falsely low A1c

A

Dapsone, ribavirin, antiretrovirals, Bactrim (MOA increased erythrocyte destruction);
hydroxyurea (MOA altered Hgb A –> F);
vitamin D, vitamin E, low dose ASA (altered glycation)

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

Medications that cause falsely high A1c

A

ASA (high dose through assay intereference), chronic opioid use (unclear MOA)

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

In patients taking an SGLT2-inhibitor, what do you measure if suspicion for euglycemic DKA is high?

A

serum beta-hydroxybutyrate. Urinary ketone excretion is limited so it is not a reliable measure.

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

Gastroparesis:

  1. symptoms
  2. diagnosis
  3. treatment
A
  1. some patients are asx. Early satiety and the feeling of fullness
  2. scintigraphy, stable isotope breath test, and motility assessment using wireless pressure and a pH capsule. Delayed gastric emptying is defined as >60% retention at 2 hrs and/or >10% at 4 hours. Do NOT evaluate if BG>275 mg/dl.
  3. nutrition consult for low-fat, low-fiber, small particle size diet
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q
  1. What atypical antipsychotic medications have adverse metabolic consequences?
  2. what other antipsychotic drugs have lesser metabolic effects? (intermediate and little/none)
A
  1. OLANZAPINE and CLOZAPINE (“old closets” make you gain weight) (wt gain, hyperlipidemia, insulin resistance, impaired glucose metabolism)
  2. intermediate: quietapine and risperidone (“quiet whispers”)
    little/none: aripiprazole, ziprasidone, amisulpride
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Non-islet cell tumor:

  1. usually present in patients with what condition?
  2. main mechanism?
  3. lab findings
A
  1. malignancy - mesenchymal tumors (fibrosarcoma) or epithelial tumors (hepatocellular carcinoma)
  2. production of excess incompletely processed IGF-2 (“big IGF-2”) –> stimulates insulin receptors and increases glucose levels –> hypoglycemia
  3. LOW plasma insulin, glucagon, and GH levels;
    IGF2/IGF1 are elevated
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Insulin autoimmune syndrome aka Hirata disease (Japanese population)

  1. characterized by?
    - how to dx?
A
  1. hyperinsulinemic hypoglycemia, elevated insulin autoantibodies in patients with no previous exposure to exogenous insulin or other pancreas pathology
    - dx by checking insulin antibody levels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Lab findings suggestive of endogenous excess insulin production? Insulin, C-peptide, beta hydroxybutyrate

A

insulin > 3 uIU/mL
C-peptide >0.6 ng/ml
beta-hydroxybutyrate <2700 umol/mL at the end of fast

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

Indications for initiating insulin

A
  • glucose greater than 300 mg/dl
  • A1c >10%
  • catabolic state (weight loss)

Basal insulin:
suppresses hepatic glucose production
stimulates glucose uptake by fat and muscle
reduces ketogenesis and risk for dka

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

treatment for NASH and DM

A

pioglitazone and liraglutide
fibrosis is also helped
No data on dulaglutide

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

Any basal insulin dose greater than [ ] does not confer additional benefit and increases risk of hypoglycemia.

A

0.5 units/kg

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

Besides diet and exercise, what medications improve insulin resistance in managing lipodystrophy?

A

pioglitazone

(improves glucose control, TG, and liver enzymes) –> by affecting serum adiponectin levels

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

Cardiovascular risk reduction in a patient with T2DM:

consists of what 3 things?

A

BP control
Lipid management
use of anti-platelet agents (ASA)

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

Cardiovascular risk reduction in a patient with T2DM:
Use of antiplatelet agents for PRIMARY prevention in -

  1. high risk
    (50+ with at least 1 risk factor for ASCVD)
  2. intermediate risk
    (50+ w/o other risk factors OR
    less than 50 yrs + at least 1 risk factor)
  3. low risk (less than 50 yo w/o other risk factors)
A

age cutoff: 50 yo

  1. use ASA for primary prevention
  2. discuss risks and benefits
  3. avoid use of ASA for primary prevention
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Cardiovascular risk reduction in a patient with T2DM:

Lipid management in a patient WITHOUT a history of ASCVD -
1. 40-79 yo
2. 20-39 yo
3. long duration of DM (T2DM > 10 yrs or T1DM > 20 years) or
evidence of microvascular disease (retinopathy, MAC > 30, eGFR <60, or peripheral neuropathy), or if patient has an ABI < 0.9

A
  1. at least moderate-intensity statin
  2. start statin if LDL > 190
  3. start at least a moderate intensity statin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Cardiovascular risk reduction in a patient with T2DM:

TG (a secondary target in patients with DM)

  1. If TG 175-499
  2. TG greater than 500
  3. icosapent ethyl can be considered in?
A
  1. lifestyle changes
  2. medication + lifestyle changes
  3. icosapent ethyl can be considered in patients with a known history of ASCVD and TG 135-499, with LDL cholesterol controlled on statin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Cardiovascular risk reduction in a patient with T2DM:

Blood pressure

  1. ADA recs in patients with:
    a. DM
    b. ASCVD risk greater than 15%
  2. AHA recs
A
  1. a. < 140/90
    b. < 130/80
  2. < 130/80 in all patients with diabetes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

10-year risk for ASCVD is categorized as:
Low-risk (% ?)
Borderline risk
Intermediate risk
High risk

A

Low-risk ( < 5%)
Borderline risk (5% to 7.4%)
Intermediate risk (7.5% to 19.9%)
High risk ( ≥ 20%)

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

MDI to pump conversion equations:

  1. pump total daily dose
  2. ICR
  3. ISF
A
  1. 0.75-1 x prepump TDD
  2. 450-500 / TDD
  3. 1700-1800 / TDD
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Causes of painful neuropathy:

POLYNEUROPATHY

What type of loss?

A

progressive SENSORY loss (starts in distal extremities and moves proximally)
Can have loss of ankle reflexes and motor dysfunction

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

Causes of painful neuropathy:

RADICULOPATHY
presentation? weakness?
a subtype of radiculopathy

A

presents in LUMBAR or THORACIC area
acute pain and MOTOR weakness
–> diabetic amyotrophy is a form of radiculopathy

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

Causes of painful neuropathy:

treatment-induced neuropathy of diabetes (also known as?)

A

aka insulin neuritis

associated with rapid improvement of blood glucose levels within 8 weeks
acute onset of neuropathic pain or autonomic dysfunction
A1c reduction of > 2% within 3 months
A small fiber neuropathy

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

Causes of painful neuropathy:

Diabetic neuropathic cachexia: occurs in what patient population?

Presentation?

A

in middle-aged or older men on oral hypoglycemic agents

severe unintentional weight loss and severe painful neuropathy

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

the triad of diabetes, diarrhea/steatorrhea, and cholelithiasis makes [what] the most likely cause of secondary diabetes?

A

somatostatinoma

seen in 10% of NF1

32
Q
  1. Nesidioblastosis is also known as?
  2. Pathology shows?
A
  1. Noninsulinoma pancreatogenous hyperinsulinemic syndrome - NIPHS
  2. diffuse islet hypertrophy and hyperplasia
33
Q

treatment of sulfonylurea-induced hypoglycemia

A

octreotide (off-label use)

34
Q
  1. In patients with acquired generalized lipodystrophy (aka Lawrence syndrome), what do you test?
  2. what is the drug approved for treatment?
A
  1. Leptin and adiponectin (both suppressed)
  2. metreleptin (a recombinant human methionyl leptin)
35
Q
  1. In asymptomatic adults, diabetes screening should be considered in patients who are?
  2. Testing in patients with prediabetes should be done?
  3. Women diagnosed with gestational diabetes should have lifelong testing at least every how many years?
A
  1. overweight or obese or who have 1 or more of the following risk factors: first-degree relative with diabetes, high-risk race/ethnicity, history of CVD, HTN, HLD < 35, and/or TG >250, PCOS, physical inactivity
  2. yearly
  3. at least every 3 years
36
Q

The ADA criteria for the diagnosis of diabetes are? (4 total)

A
  1. hgb A1c > or equal to 6.5% OR
  2. Fasting plasma glucose > or equal to 126 mg/dl OR
  3. Two-hr OGTT plasma glucose > or equal to 200 mg/dL after a 75 g load OR
  4. In a patient with classic symptoms of hyperglycemia or hyperglycemic crisis, a random plasma glucose value > or equal to 200 mg/dL *In the absence of unequivocal hyperglycemia, criteria 1 to 3 should be confirmed by repeat testing
37
Q

In patients with hemoglobinopathies (such as sickle cell disease or other causes or increased RBC turnover), what should be measured?

A

Fructosamine (which is a measure of glycosylated plasma proteins, proportional to the mean blood glucose over the previous 2 weeks)

38
Q

Case: A patient with T1DM develops unpredictable blood glucose measurements and recurrent episodes of hypoglycemia. What to test for?

A

TTg IgA (Celiac disease) = causes erratic intestinal absorption of nutrients

39
Q

Risk of T1DM in the following: 1. No family hx 2. offspring of an affected parent 3. offspring of BOTH affected parents

A
  1. 0.4% 2. 4-8% (having an affected father confers a higher risk than having an affected mother) 3. up to 30%
40
Q

calculations for conversion from MDI to insulin pump: 1. How to calculate pump TDD using MDI TDD 2. How to calculate pump TDD using weight based 3. Calculation for basal rate? 4. Calculation for ICR? 5. Calculation for ISF?

A
  1. pre-pump TDD x 0.75 2. weight: kg x 0.5 or lb x 0.23 3. basal rate: (pump TDD x 0.5)/24 h Start with one basal rate. Adjust according to glucose trends over 2-3 days. Adjust to maintain stability in fasting state (between meals and during sleep). Add additional basal according to diurnal variations (dawn phenomenon) 4. ICR = 450/TDD Adjust based on low-fat meals with known CHO content. Acceptable 2-hr postprandial rise is ~60 mg/dL above preprandial BG. Adjust CR in 10-20% increments based on post-prandial BG. alternative = fixed meal bolus = (TDD x 0.5)/3 meals when not carb counting. Continue existing CR approach from MDI regimen 5. ISF = 1700/Pump TDD To assess sensitivity factor, BG should be checked 2 h after correction: if BG is within 30 mg/dL of target range, sensitivity is correct. Make adjustments in 10-20% increments if 2-h post correction BGs are consistently above or below target
41
Q

The mechanism of action of SGLT2-inhibitors is?

A

To reduce filtered glucose reabsorption in the proximal tubule, therefore lowering the renal threshold for glucose excretion from 220 mg/dL to < 100 mg/dL.

“STICH” protocol in euglycemic DKA:
STop SGLT2 inhibitor treatment
Insulin administration
Carb consumption
Hydration with water or sugar-free electrolyte drink

42
Q

What intervention will most likely result in complete resolution of diabetes-related necrobiosis lipoidica?

A

Pancreas transplant +/- a kidney transplant

43
Q

Case: Findings on abdominal CT of significant subcutaneous air and edema in the left lateral anterior abdominal wall tracking into the left groin and extending into the perineum. an aggressive form of necrotizing fasciitis due to mixed aerobic and anaerobic organisms that affects the perineal and genital region. What this called?

A

Fournier gangrene uncontrolled diabetes, immunosuppressed states, and obesity often contribute to its rapid progression.

44
Q
  1. Diabetes-related muscle infarction is also known as?
  2. symptoms?
  3. lab findings?
  4. MRI findings?
  5. Pathogenesis?
  6. Treatment?
A
  1. muscle ischemia or spontaneous myonecrosis
  2. acute or subacute pain, swelling, and tenderness, typically in the thigh or in the calf.
  3. nonspecific and normal. Some may have elevated CK, ESR, and WBC.
  4. high intensity T2, and hypointense/isointense T1
  5. Vasculopathy associated with longstanding, suboptimally controlled diabetes
  6. symptomatic management with rest, optimal glycemic control, analgesia, and low-dosage aspirin.
45
Q
  1. Acquired partial local lipodystrophies include?
  2. Treatment and MOA?
A
  1. lipoHYPERertrophy and lipoAtrophy at insulin injection sites. Insulin absorption from these sites is unpredictable and can lead to erratic glycemic control and an increased predisposition to severe hypoglycemia. Mast cells overproduce cytokines and TNF which inhibit adipocyte differentiation. Failure to rotate insulin injection sites and reuse of needles are associated with risk for lipoatrophy.
  2. sodium cromolyn, which is a mast-cell stabilizer
46
Q

In unprovoked hypoglycemia in patients with preexisting autoimmune disease (such as Graves disease), the possibility of what disease should be considered?

A

insulin autoantibody syndrome (Hirata disease) : autoantibodies (IgG) are produced that bind insulin with variable affinity, which may result in glucose intolerance. Sudden dissociation of prebound insulin from the antibody results in unpredictable episodes of hypoglycemia. Can be a rare adverse reaction to methimazole, and almost all cases of methimazole-induced insulin autoimmune syndrome are reported in East Asia, especially in Japan. Due to the DRB1*0406 genotype. Measure both C peptide and insulin levels

47
Q

In a patient with diabetes, arterial calcification makes the diagnosis of peripheral arterial disease by ankle brachial index alone less reliable, so the diagnosis should be confirmed by sending this patient to?

A

vascular lab to have vascular segmental pressures and pulse volumes checked

48
Q

Treatment for insulinoma (immediate then maintenance)

A
  1. diazoxide: directly inhibits insulin production and secretion. Adverse effects include GI, edema, hirsutism 2. mainstay of therapy: short-acting somatostatin-based treatments (such as octreotide TID).
49
Q

at initial diagnosis, what test is recommended for all women with polycystic ovary syndrome?

A

A 2-hour oral glucose tolerance test with measurement of fasting and 2-hour glucose. If this is not feasible, fasting glucose should be measured together with hemoglobin A1c.

50
Q

Up to 20% of patients with type 1 diabetes have positive [] antibodies?

A

antithyroid antibodies (TPO and/or thyroglobulin antibodies)

51
Q

certain antidiabetes agents have been shown to improve liver histology such as steatosis, lobular inflammation, hepatocellular ballooning, and fibrosis. What are they? (2)

A

Pioglitazone and liraglutide (Victoza)

52
Q
  1. For a patient with HHS/DKA, starting IV bolus of regular insulin is? And starting continuous infusion of regular insulin is?
  2. what criteria should be met to ensure that DKA has resolved?
A
  1. 0.1 units/kg body weight and 0.1 units/kg/hr
  2. serum glucose < 200 mg/dl + 2 of the following (serum bicarb > 15; pH > 7.3; AG < 12 for 8-12 hrs). After meeting these can a pt transition off an insulin gtt (overlap for 2 hrs)
53
Q

what is LADA by definition?

A

-onset after 30 years
-with at least 6 month initial treatment period without insulin and
-elevation in autoimmune markers such as GAD Ab

54
Q

use of fenofibrate reduces the need for what diabetes related complication?

A

Laser photocoagulation (hazard ratio, 0.69) and is associated with less macular edema (hazard ratio, 0.66) and less progression of diabetic retinopathy

SBP lowering from 154 to 144 can also help diabetic retinopathy, but nothing below this.

55
Q

What is the classic presentation of Type 4 RTA?

A

Mild-moderate renal insufficiency due to diabetic nephropathy; mild, normal anion gap metabolic acidosis in a patient 50-70 yo; Due to diabetic nephropathy. Therefore renin and aldosterone are LOW. ACTH and cortisol are normal. Hyperkalemia may occur in the absence of potassium-raising antihypertensive agents, or commonly worsened by their use.

56
Q

At initial diagnosis of PCOS, what is the recommended and most sensitive test to evaluate a patient’s risk for diabetes? If this is not feasible, what other tests can be done?

A

2-hour OGTT; If this is not feasible, a fasting glucose and hemoglobin A1c should be measured If normal, screen at least every 2 years

57
Q

DDX of hyperkalemia in a patient with T2DM?

A

use of an ACEi, renal insufficiency, adrenal insufficiency, isolated hypoaldosteronism NOTE: -ACEi use leads to acute low aldosterone levels. However, with long term use, there is incomplete suppression of aldosterone (“aldosterone breakthrough”) since angiotensin II is being made through alternative pathways.

58
Q

What states cause a falsely low fructosamine?

A

In states with a rapid albumin turnover:

  • protein-losing enteropathy or
  • nephrotic syndrome
59
Q
  1. Hemoglobin A1c recommendations in PREGNANCY?
  2. Recommendations by ACOG and ADA glucose targets:

Fasting?

Premeal?

1-hour pp?

2-hour pp?

Nocturnal?

A
  1. ACOG: <6%

ADA: 6-6.5 in early pregnancy

Relax glucose control in patients with hypoglycemia unawareness

  1. Fasting <95 mg/dL

Premeal <100

1-hour pp <140

2-hour pp <120

Nocturnal >60

60
Q

What tests should be ordered to assess for the need for insulin treatment 12 months after presenting in DKA?

A

(known as the Aß system)

  • GAD 65 Ab or Islet-cell autoantibodies
  • C peptide
61
Q
  1. What is type B insulin resistance?
  2. clinical features?
  3. Why is this important?
  4. Treatment?
A
  1. An autoimmune condition in which antibodies to the insulin receptor develop.
  2. extreme insulin resistance, extensive acanthosis, low serum TG level. Affected persons are typically middle-aged, nonobese black women with acanthosis nigricans, and they often have other rheumatologic conditions.
  3. It is associated with high mortality – as high as 54%.
  4. rituximab, cyclophosphamide, and dexamethasone followed by maintance azathioprine. Associated with long-term remission of diabetes and freedom from insulin requirement.
62
Q

Medications that cause falsely low A1c

A
  • Increased erythrocyte destruction: dapsone, ribavirin, antiretrovirals, Bactrim
  • altered hemoglobin: Hydroxyurea (HgA -→ HgF)
  • altered glycation: Vitamins D & E, low dose aspirin
63
Q

Medications that cause falsely high hemoglobin A1c

A

high dose aspirin, chronic opioid use

64
Q

Treatments for gastroparesis

A
  1. metoclopramide (MOA - central dopa receptor antagonist)
  2. domperidone - (same MOA as above); does not cross BBB so has fewer extrapyramidal SEs, but with greater cardiac effects (prolongs QT interval)
  3. erythromycin - (motilin receptor agonist)
65
Q

MODY:

What are the most common (99%) cases of MODY? Describe each.

A

MODY 1 - HNF4A (10%)
MODY 2 - GCK (15-35%)
MODY 3 - HNF1A (50-65%)

Both MODY 1 and 3 present with hyperglycemia and glucosuria. Can initially treat with SU, then may require insulin. + complications

MODY 2 defect is beta cell glucose sensing. No vascular complications. Tx is diet.

Other MODY’s (rare):
MODY 4 (PDX1): pancreas agenesis; Tx is insulin
MODY 5 (HNF1B): can present with abnormal kidney development or pancreatic atrophy; low mag; Tx is insulin
MODY 6 (NEUROD1): tx is insulin

66
Q

Lab findings suggestive of endogenous insulin production

A

insulin > 3 uIU/mL

C-peptide >0.6 ng/ml

B-hydroxybutyrate <2700 umol/L

67
Q

Dosing of different types of insulin:

  1. NPH
  2. Levemir/detemir
A
  1. Give ⅔ in the am and ⅓ in the pm
  2. at doses less than 0.3 units/kg, give twice daily
68
Q

What is an acceptable % of device use for data interpretation for a patient using a CGM?

A

greater than 70%

69
Q

T1DM and exercise: to reduce the chance of hypoglycemia, what is recommended?

A

Consider a brief period of weightlifting before jogging to reduce the chance of hypoglycemia.

70
Q

insulin degludec:
1. best suited for?
2. duration of action and when to administer

A
  1. travel/erratic schedule
  2. 42 hours; can administer 8-40 hours between doses
71
Q

what types of diplopia can patients with diabetes develop?

A

isolated 3rd (oculomotor), 4th (trochlear) or 6th (abducens) nerve palsy

72
Q

Clinical features of patients with ketosis prone diabetes

A
  • present with an episode of DKA
  • obese
  • insulin resistant
  • usual phenotype of T2DM
  • most present in the 2nd or 3rd decade of life
  • can stop insulin after recovery of beta cells
73
Q

In patients with T2DM, most common causes of hyperkalemia include:

A

the use of an ACEi, renal insufficiency, adrenal insufficiency, isolated hypoaldosteronism

74
Q
  1. what is the classic presentation of type 4 RTA?
  2. lab values?
A
  1. mild, normal anion gap metabolic acidosis in a patient 50-70 yo with mild to moderate renal insufficiency due to diabetic nephropathy
  2. low renin and aldosterone, normal cortisol and ACTH
75
Q

criteria for the diagnosis of HHS

A
  1. plasma glucose > 600 mg/dl
  2. serum Osm > 320
  3. pH > 7.30
  4. bicarb > 18
  5. severe dehyration without/minimal ketoacidosis
76
Q

Secondary diabetes
1. definition
2. categories

A
  1. occurs when a separate condition leads to hyperglycemia; these are considered distinct from routine type 1 or 2 diabetes
    • medication induced (corticosteroids)
    • other endocrinopathies (acromegaly)
    • pancreatic diseases (pancreatitis)
    • infections (CMV)
    • genetic conditions (primary hemochromatosis, Rabson-Mendenhall syndrome)
    • secondary hemochromatosis due to increased RBC breakdown (thalassemia, many blood transfusions, sideroblastic anemia, hemolytic anemia)

Endocrinology (8 decks)

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