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Step 1 Journal RC > DIT Part 2 > Flashcards

DIT Part 2 Flashcards

1
Q

What happens in ketogenesis

A

in the liver, Fatty acids and Amino Acids are metabolized to acetoacetate and then (with NADH) to beta-hydroxybutyrate. These are to be used in muscle and brain

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2
Q

What are the main ketone bodies

A

Acetoacetate

Beta-hydroxybutyrate

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3
Q

RLS for ketone synthesis

A

HMG-CoA synthase (NOT REDUCTASE)

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4
Q

Acetoacetate sponteously becomes

A

Acetone

note the fruity smell to breath

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5
Q

Urine test for ketone bodies tests for

A

Tests for Acetoacetate

NOT beta-hydroxybutyrate

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6
Q

Why does drinking alcohol stop gluconeogenesis

A

Liver regenerates NAD+ by converting pyruvate to lactate

converting oxaloacetate to malate

resulting in a severe fasting hypoglycemia by patients who consume a lot of alcohol in a fasting state

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7
Q

what can the body do with acetyl-CoA

A

TCA cycle
FA synthesis
Cholesterol synthesis
Ketone synthesis

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8
Q

What is seen in kwashiokor

A

FLAME

  • Fatty Liver (no production of ApoB-100, to make particles with cholesterol and triglycericdes)
  • Anemia
  • Malnutrition
  • Edema

(also skin lesions and depigmentation of skin and hair)

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9
Q

what happens in Refeeding syndrome?

A

drop in serum levels of mg, phosphate potassium which can lead to arrhythmias and neurological problems

Overall depletion of ATP

Why you need to take it slow and monitor

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10
Q

What are risks for hepatocellular carcinoma

A 
Hep B and C
Hemochromatosis
alpha1-antitrypsin deficiency
Hepatic adenoma
Any type of Cirrhosis
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11
Q

TCA overdose symptoms

A

convulsions
coma
cardiotoxicity

hyperpyrexia
respiratory depression

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12
Q

Apo B-48

A

Chylomicron secretion from enterocyte to lymphatic system

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13
Q

ApoB-100

A

Found on VLDL, IDL, and LDL

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14
Q

Apo E

A

Mediates extra remnant uptake

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15
Q

Apo A-I

A

Activates LCAT, found on HDL

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16
Q

Apo C-II

A

Cofactor for lipoprotein lipase

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17
Q

Chlylomicron has what apoproteins

A

Apo E, Apo A-I, Apo C-II, Apo B-48

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18
Q

Chylomicron remnant has what apoproteins

A

Apo E, Apo B-48

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19
Q

VLDL has what apoproteins

A

Apo E, Apo C-II, Apo B-100

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20
Q

IDL has what apoproteins

A

Apo E, Apo B-100

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21
Q

LDL has what apoproteins

A

Apo B-100

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22
Q

HDL has what apoproteins

A

Apo E, Apo A-I Apo C-II

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23
Q

Abetalipoproteinemia mechanism

Presentation

A

Autosomal recessive disorder with decrease in ApoB-48 and ApoB-100

mech: inability to generate chylomicrons, cecreased secretion of cholesterol, VLDL into bloodstream, fat accumulation in enterocytes

Presents w/

  • Failure to thrive in early childhood
  • Steatorrhea
  • acanthocytosis (spikey RBC due to alteration in membrane lipids)
  • ataxia
  • night blindness
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24
Q

treatment of abetalipoproteinemia

A

Vitamin E

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25
Q

Type I hyperchylomicronemia

Mechanism

Presentation

Is it a risk factor for atherosclerosis

A

Autosomal recessive

Mech: Deficiency of lipoprotein lipase
or
Defective apolipoprotein C-II

Presentation: Pancreatitis (from increased triglycerides), hepatosplenomegaly, pruritic xanthomas

No increased risk for atherosclerosis

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26
Q

Type IIa familial hypercholesterolemia

Mechanism

Presentation

A

Autosomal dominant

Mech: Absent or decreased LDL receptors.

Presents with Tendinous xanthomas (achilles), Corneal arcus, accelerated atherosclerosis, MI in 20s (for double dominant mutation)

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27
Q

Type IV hypertriglyceridemia

Mech:

Presentation

A

Autosomal dominant

Mech: Overproduction of VLDL

Pancreatitis (from increased triglycerides)

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28
Q

Signs of hyper cholesterolemia

A

Atheromas, plaques in blood vessel wall-oxidized LDL

Xanthomas- plaques or nodules of histiocytes filled with lipid. esp around eyelid.

Xanthelasma-xanthoma on eyelid

Tendinous xanthomas-commonnly achilles, elbows,

Corneal arcus-lipid deposition in the cornea

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29
Q

Fatty acid synthesis:

Precursor,Location, RLS

A

Acetyl-CoA is precursor, occurs in cytoplasm of hepatocytes, RLS is Acetyl-CoA carboxylase

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30
Q

Fatty acid degrdation:

Location

RLS

A

located in mitochondria, RLS is Carnitine acyltransferase-1 (aka carnitine palmitoyl transferase-1)

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31
Q

What is seen in carnitine deficiency? mechanisms and presentation

A

Inability to transport long chain fatty acids into the mitochondria, resulting in toxic accumulation

Presents as weakness, hypotonia, hypoketotic hypoglycemia.

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32
Q

What are the essential amino acids

A

Private (PVT) TIM HaLL

  • Phenylalanine
  • Valine
  • Threonine
  • Tryptophan
  • Isoleucine
  • Methionine
  • Histidine
  • Arginine
  • Leucine
  • Lysine
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33
Q

Basic AAs

A

Lysine and arginine (extra ammonia group, positve charge at body pH)

Histidine (although basic, has no charge at body pH)

Arginine and histidine (during periods of growth)

Arginine and lysine (NLS, high concentrations in histones)

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34
Q

Acidic AAs

A

Aspartate and glutamate

-negatively charged

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35
Q

Phenylalanine to Epi

A 
Phenylalanine
Tyrosine
Dopa
Dopamine
NE
Epi
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36
Q

What can arginine be turned into

A

Creatine
Urea
Nitric oxide

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37
Q

Vitamin B6 dependent AA derivatives

A

Ia. Tryptophan to Niacin to NAD/NADP
Ib. Tryptophan to Serotonin to Melatonin

II. Histidine to Histamine

III. Glycine to porphyrin to Heme

IVa. Glutamate to GABA
IVb. Glutamate to Glutathione

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38
Q

RLS for Heme synthesis

A

Aminolevulinic synthase

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39
Q

Urea cycle RLS

A

Carbamoyl phosphate synthetase- I

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40
Q

CPS I vs. CPS II

A

CPS I gets nitrogen from ammonia, works in the mitochondria, and is in the urea cycle

CPS II gets nitrogen from glutamine, works in the cytosol, and is in the pyrimidine synthesis

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41
Q

Ornithine transcarbamylase deficiency

Presentation

A 
Most common urea cycle disorder.
X linked recessive
Present in first few days of life
Orotic acid in the blood and urine 
BUN is going to be decreased
Hyperammonemia
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42
Q

Symptoms of hyperammonemia

A 
Slurring of speech
Somnolence
Vomiting
Cerebral edema
Blurring of the vision
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43
Q

Treating hyperammonemia

A

Low protein diet

If urea cycle problem:
Phenylbutyrate
Benzoate
Biotin (stimulate ornithine transcarbamylase)

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44
Q

PKU causes

A

2 ways
either missing phenylalanine hydroxylase
or
missing BH4 (tetrahydrobiopterin)

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45
Q

Why do you get neurotoxic effects in PKU

A

from high levels of phenylalanine, not due to phenylketones

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46
Q

what are the phenylketones

A

phenylacetate
phenyllactate
Phenylpyruvate

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47
Q

s/s of pku

A 
growth retardation
mental retardation
seizures
fair skin (no melanin)
eczema
musty body odor
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48
Q

dx of pku

tx

A

screen at 2-3 days

treat within first 3 wks of life

tx: avoid phenylalanine (aspartame, dairy products,), augment tyrosine into diet, BH4 supplement could be necessar.

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49
Q

What happens to infant in gestational pku

A

phenylketones are toxic

  • microcephaly
  • intellectual disability
  • growth retardation
  • congenital heart defects
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50
Q

Alkaptonuria mechanism

A

congenital autosomal recessive and benign deficiency of homogentisate oxidase in the degradative pathway of tyrosine to fumarate.

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51
Q

s/s in alkaptonuria

A

dark connective tissue, brown pigmented sclerae, urine turns black on prolonged exposure to air. Debilitating arthralgias

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52
Q

Albinism causes

A
  • Tyrosinase deficiency
  • Defective tyrosine transport
  • Abnormal neural crest migration of melanocytes
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53
Q

what is a consequence of albinism

A

skin cancer more likely

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54
Q

Homocystinuria causes

A
  1. Deficiency of cystathionine synthase
  2. Decreased affinity of the cystathionine synthase for the pyridoxal phosphate
  3. Deficiency of homocysteine methyltransferase
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55
Q

S/S homocystinuria

A 
mental retardation, 
tall stature,
osteoporosis
kyphosis
Atherosclerosis
Subluxation of the lens (downward dislocation, c/f with marfans with upward dislocation
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56
Q

Cystinuria cause

A

defect of the renal tubular AA transporter for COLA (cysteine, ornithine, lysine, arginine), normally in the convoluted proximal tubule

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57
Q

s/s of cystinuria

tx

A

Cysteine kidney stones

tx: acetazolamide to prevent

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58
Q

Maple syrup urine disease cause

A

Deficiency of branched chain alpha-ketoacid dehydrogenase complex supposed to break down..

Isoleucine
Leucine
Valine

alpha ketoacids build up in the urine and blood

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59
Q

maple syrup urine disease s/s

A

intellectual deficiencies

Severe CNS defects

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60
Q

Hartnup cause

A

Autosomal recessive defect of transporter in intestine and kidneys leading to deficiency of neutral AA (tryptophan)

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61
Q

Hartup s/s

A

Pellagra (vitamin B3 deficiency)
Dermatitis
Diarrhea
Dementia

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62
Q

Vitamin D toxicity causes

A

Too much vitamin D supplementation

Sarcoidosis (increase in conversion of 25-OH D3 to 1,25-OH D3)

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63
Q

Vitamin K deficiency causes

A

Medications

  • Coumadin
  • Anticonvulsants (phenytoin)
  • Antibiotics
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64
Q

Types of Vitamin A

A

Retinol
Retinal
Beta-carotene (cleaved in intestine to 2 molecules of retinol)
Retinoic acid not useful in body, but useful for treatment of certain diseases

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65
Q

Uses for Vitamin A

A

Mild to moderate acne (tretinoin)
Mild severe acne (isotretinoin)
[decrease size and secretion of sebaceous glands]

Measles treatment

AML (M3 subtype)

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66
Q

Vitamin A deficiency

A

Night blindness

Xerophthalmia (pathologic dryness of conjunctiva and cornea resulting in –>corneal ulcerations and blindness)

Keratomalacia (wrinkling and clouding of the cornea)

Bitot spots (bulba conjucntiva, dry silvery gray plaques)

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67
Q

Vitamin A toxicity

A

headache

N/V

Stupor

Increase in ICP (pseudotumor cerebri)

Dry and pruritic skin

Beta carotene skin orange which is not toxic.

Hepatomegaly

Cirrhosis

Bone and joint pain

Alopecia

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68
Q

What presentation of vitamin A toxicities can be seen

A

livers of bears (polar bears, or otherwise)

Pregnant mothers (teratogenic)

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69
Q

Vitamin E other name

A

alpha-tocopherol

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70
Q

What does vitamin E do

A

antioxidant, prevents non-enzymatic oxidation of cell components by free radicals (especially important for RBC)

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71
Q

vitamin E deficiency

A

hemolytic anemia

spinocerebellar degeneration resulting in ataxia

peripheral neuropathy and proximal muscle weakness

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72
Q

Vitamin C metabolic actions

A

hydroxylation of prolyl and lysyl residues of collagen

Converts dopamine to norepinephrine (required for enzyme dopamine beta hydroxylase)

Anti-oxidant

Facilitates iron absorption in the gut (keeps iron in reduced more easily absorbed state)

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73
Q

Scurvy/vit c deficiency

A 
sore spongy gums
loose teeth
fragile blood vessels
swollen joints
hemarthrosis
impaired wound healing
anemia
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74
Q

What is the ddx for eosinophilia

A

DNAAACP

Drugs
Neoplasm
Atopic disease
Addison's disease
Acute interstitial nephritis
Collagen vascular disease
Parasites
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75
Q

What requires vitamin B1 (thiamine)

A

PDH

alpha-ketoglutarate dehydrageonase

transketolase

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76
Q

What are consequences of thiamine deficiency

A

Wernicke-Korsakoff
Dry beriberi
Wet beri beri

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77
Q

What is dry beriberi

A 
nonspecific peripheral neuropathy with myelin degeneration
toe drop
wrist drop
foot drop
muscle weakness
hyporeflexia
areflexia
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78
Q

what is wet beriberi

A

Peripheral vasodilation
High output heart failure
Peripheral edema
Cardiomegaly

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79
Q

B2 (riboflavin) deficiency symptoms

A

Cheilosis (inflammation of lips, scaling and fissures at the corners of the mouth)
Corneal vascularization

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80
Q

B3 (niacin) deficiency symptoms

A

glossitis

Pellagra
Diarrhea
Dementia
Dermatitis

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81
Q

causes of niacin deficiency

A

Hartnup disease (decrease tryptophan absorption)

Malignant carcinoid syndrome (increase tryptophan metabolism)

INH (inhibits B6 and B3)

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82
Q

What can Niacin be used to treat

A

dyslipidemia, b/c increase HDL and decrease LDL.

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83
Q

Side effect of taking niacin?

A

Flushing rxn, which you can take aspirin 30 minutes prior

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84
Q

What is B5 used for

A

component of coenzyme A, transfer of acyl groups

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85
Q

Deficiency in B5

A

dermatitis
enteritis
alopecia
adrenal insufficiency

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86
Q

metabolic fxn of B6

A

(Pyridoxal phosphate) coenzyme for numerous enzymes, transaminations, deaminations.

converting AA precursors into…

heme niacin histamine gaba dopamine NE EPI

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87
Q

B6 deficiency

A

similar to riboflavin (angular cheilosis, glossitis)

unique is convulsions and hyperirritability and peripheral neuropathy

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88
Q

What can cause deficiency in B6

A

INH (same as B3)

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89
Q

B7 (biotin) role

A

apoenzyme for carboxylation reactions

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90
Q

B7 deficiency causes

A

Avidin in egg whites prevents absorption

antibiotics

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91
Q

B9 (folic acid) fxn

A

synthesis of DNA and repair of DNA

Synthesis of purines and pyrimidines

rapid cell division and growth

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92
Q

Biologically active form of folic acid

A

tetrahydrofolate

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93
Q

how does b9 deficiency occur

A

medications

  • phenytoin
  • sulfonamides
  • TMP
  • MTX

malnutrition

Pregnancy (rapid growth of fetus)

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94
Q

B9 deficiency

A

Glossitis
Diarrhea
Depression
Confusion

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95
Q

DNA virus characteristics

A

Double stranded
Linear genomes
Icosahedral
Replicate in the nucleus

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96
Q

Exceptions to the DNA virus characteristics

what are the DNA virus characteristics

A

Papillomavirus/Polyomavirus/Hepadnavirus: have circular DNA

Parvovirus is ssDNA

Poxvirus is non-icosahedral

Poxvirus replicates in cytoplasm

Double stranded
Linear genomes
Icosahedral
Replicate in the nucleus

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97
Q

Live virus vaccines

A 
Smallpox
Yellow fever
Chicken pox (varicella)
MMR
Sabine polio vaccine (oral)
Herpes zoster vaccine
Intranasal influenza
Rotavirus
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98
Q

killed virus vaccine

A

injectable influenza
rabies
hepatitis A
injectable Salk polio

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99
Q

Subunit vaccine

A

Hepatitis B

Human papillomavirus

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100
Q

Egg allergy concerns for vaccines

A

Yellow fever: skin test/desensitization
Influenza: if no anaphylactic egg response
MMR: no CI

How well did you know this?
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101
Q

Non-enveloped RNA virus

A

Calicivirus
Picornavirus
Reovirus
Hepevirus

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102
Q

Non-enveloped DNA virus

A

Parvovirus
Adenovirus
Papillomavirus
Polyomavirus

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103
Q

Viral reassortment, what is it

what does it

what is the consequence

A

among segmented genome RNA viruses, exchange genetic segments.

shown in influenza.

can have pandemics/epidemics due to significant change in surface antigens

104
Q

Viral recombination

found in what

A

Genes exchanged. progeny unlike progenitors

found in DNA or RNA with DNA phase

105
Q

Phenotypic mixing

A

Surface protein packaging is mixed. only works for the first generation of progeny.

106
Q

What is the ploidy of viruses

A

Haploid

Except Retrovirus have 2 copies of ssRNA

107
Q

RNA viral genomic structure normally is

exceptions

A

Most ssRNA

Reovirus and Rotavirus have dsRNA

108
Q

Positive sense RNA virus

A 
Picornavirus
Hepevirus
Calicivirus
Flavivirus
Togavirus
Coronavirus
Retrovirus
109
Q

Negative sense RNA virus

A 
Orthomyxovirus
Paramyxovirus
Rhabdovirus
Filovirus
Bunyavirus
Arenavirus
Reovirus (dsRNA)
110
Q

What can infect cells just by using their naked genome?

Exceptions?

A

most dsDNA virus and ssRNA positive

Poxvirus and hepatitis B are exceptions

111
Q

What is pulsus paradoxus

causes?

A

when Systolic BP drops by >10 mmHg with inspiration

Caused by when the lungs are hyperinflated:

  • Asthma
  • COPD
  • Cardiac tamponade
112
Q

what is the most common tumor of adrenal medulla in kids and what does it cause

A

Adrenal neuroblastoma

Does not cause episodic HTN,

can cause sustained HTN

113
Q

What can ketoconazole mechanistically do aside from antifungal

A

Inhibits desmolase

Inhibits 11beta-hydroxylase

(antiandrogen and antiglucocorticoid)

114
Q

What is ketoconazole used for aside from antifungal?

A

2nd line treatment for advanced prostate cancer and for

suppresion of glucocorticoid synthesis in treating Cushing’s syndrome

115
Q

What features characterize a deficiency in 3beta-hydroxysteroid dehydrogenase

A

Inability to produce:

  • glucocorticoids
  • mineralocorticoids
  • androgens
  • estrogens

Excessive sodium excretion in the urine

Early death

116
Q

What features characterize a deficiency in 17alpha-hydroxylase

A

Inability to produce sex hormones and cortisol–>phenotypic female who is unable to mature

Increased production of mineralocorticoids–>HTN

117
Q

What features characterize a deficiency in 11beta-hydroxylase

A

Inability to produce:

  • Cortisol
  • Corticosterone
  • Aldosterone

Increased production of deoxycorticosterone (weak mineralocorticoid)–> HTN

Increased production of sex hormones–>

118
Q

What features characterize a deficiency in 21 alpha-hydroxylase

A

Inability to produce cortisol–>elevated ACTH

Inability to produce mineralocorticoids–>hypotension and salt wasting

Increased production of sex hormones–>masculinization

119
Q

what patient groups must avoid fluoroquinolones

A

children
pregnant women
(joint and cartilage toxicity)

120
Q

Causes of Cushing Syndrome

A
  • Exogenous steroid use
  • ACTH producing pituitary adenoma (cushing disease)
  • Ectopic ACTH production (small cell lung cancer)
  • Cortisol producing adrenal adenoma
121
Q

Glucocorticoid toxicity symptoms

A

BAM, CUSHINGOID

buffalo hump
amenorrhea
moon facies
crazy
ulcers
skin changes
hypertension
infection
necrosis of femoral head
glaucoma (and cataracts)
osteoporosis
immunosuppression
diabetes
122
Q

what is glucocorticoids antiinflammatory response from (mechanism)

A

Inhibits cyclooxygenase and phospholipase A2

123
Q

What does cortisol do

A

Maintains BP (upregulate alpha1 arteriole receptors)

Increase gluconeogenesis

Increase lipolysis

Increase proteolysis

Suppresses immune system

Suppresses inflammation

124
Q

why use dexamethasone for testing cause for excess cortisol?

A

dexamethasone test, this works b/c does not interfere with the cortisol assay

125
Q

Most common causes of cushing syndrome

A

Exogenouse steroid use
Ectopic ACTH secretion
ACTH secreting pituitary adenoma
Adrenal tumor that secretes cortisol

126
Q

what is treatment for nephrogenic diabetes insipidus and how do these treatments work

A

Hydrochlorothiazide-help concentrate urine

Amiloride-treats nephrogenic diabetes insipidus caused by lithium toxicity (by closing ENac channels that lithium comes in through)

Indomethacin-reduce renal blood flow

127
Q

how do acidosis and alkalosis affect extracellular potassium concentrations

why does this occur

A

Acidosis is higher extracellular K+ concentration

Alkalosis is decreased extracellular K+ concentration

cells have a H+/K+ countertransport

128
Q

Schizotypal

A

personality disorder with interpersonal awkwardness, odd thoughts, odd appearance, strange behavior

129
Q

Schizophrenia

A

delusions or hallucinations with or without negative symptoms

Greater than 6 months

130
Q

schizoaffective disorder

A

schizophrenia symptoms with mood disorder

131
Q

schizoid

A

personality disorder with voluntary social withdrawal

132
Q

schizophreniform

A

schizophrenia symptoms that last more than 1 month but fewer than 6 months

133
Q

What are causes of secondary hyperaldosteronism

A

Renal artery stenosis
Congestive heart failure
Low protein states (cirrhosis or nephrotic syndrome)

134
Q

what is pheochromocytoma associated with

A

MEN 2A and 2B
Neurofibromatosis I
EPO->polycythemia

135
Q

What tumors can secrete erythropoietin

A

Pheochromocytoma
Renal cell carcinoma
Hemangioblastoma
Hepatocellular carcinoma

136
Q

treatment for pheochromocytoma

A

First alpha blocker (phenoxybenzamine)

Second, beta blocker for reflex tachycardia.

Third, surgical resection

DO NOT DO BETA BLOCKER FIRST BECAUSE THIS CAN RAISE BP HIGHER.

137
Q

Adrenal neuroblastoma is what

A

tumor of sympathetic ganglion cells

most common tumor of adrenal medulla in children.

138
Q

What does adrenal neuroblastoma cause

how can you dx?

A

not episodes as pheochromocytoma, but causes mild HTN

Monitor HVA and VMA for diagnosis

139
Q

Associations with adrenal neuroblastoma?

A

N-myc oncogene
Bombesin tumor mark
Neurofilament stain
Homer wright pseudorosettes

140
Q

What does MEN 1 cause

A

-Parathyroid adenoma
-Pituitary adenoma
-Pancreatic tumor (leading to..
Gastrinoma
Insulinoma
Glucagonoma
VIPoma)

141
Q

What does MEN2A cause

A
  • Medullary thyroid cancer
  • Pheochromocytoma
  • Parathyroid hyperplasia (not adenoma as in MEN1, all the glands are a problem not just the one)
142
Q

What does MEN2B cause

A
  • Medullary thyroid cancer
  • Pheochromocytoma
  • Oral and intestinal ganglioneuromatosis (mucosal neuromas)
143
Q

What gene is associated with MEN2A and MEN2B

A

RET oncogene

144
Q

Presentation of Addison disease

A 
Hypotension
Hyponatremia
Hyperkalemia
Weakness
Malaise
Anorexia
Weight loss
Skin hyperpigmentation
145
Q

Cause of Addison disease

A

Autoimmune destruction of adrenal glands leading to decreased production of aldosterone and cortisol

146
Q

MEN1
MEN2A
MEN2B

what tumor locations are associated with these 3 different types of multiple endocrine neoplasia

A

Parathyroid
Pituitary
Pancreas

Parathyroid
Pheochromocytoma
Medullary thyroid cancer

Pheochromocytoma
Medullary thyroid cancer
Mucosal neuroma

147
Q

What would a lab detect in the plasma and urine of a patient with pheochromocytoma?

A

plasma

  • metanephrine
  • normetanephrine

urine
-VMa (vanillylmandelic acid)

148
Q

Most common tumor of the adrenal

A

benign, non-functioning adrenal adenoma

149
Q

Most common cause of primary aldosteronism

A

Adrenal adenoma (conn syndrome)

150
Q

Conn syndrome presentation

A

(hyperaldosteronism)

  • HTN
  • Hypokalemia
  • Metabolic alkalosis
151
Q

why does primary hyperaldosteronism cause metabolic alkalosis

A
  1. Decreased potassium leads to urinary H+ loss

2. As potassium goes down, cells try to pump potassium out and inherently H+ in via the cotransport

152
Q

Stages of behavioral change

A 
I. Precontemplation
II. Contemplation
III. Preparation
IV. Action
V. Maintenance
153
Q

What is the characteristic sequence of the promoter region

A
  • 25: TATA box (Hogness box)

- 75: CAAT

154
Q

What does a mutation in the promoter region cause

A

decrease in transcription of gene

155
Q

Which causes of vaginal discharge/vaginitis will the pH be high?

In which will the pH be low?

A

Low pH (normal)

  • Physiologic discharge
  • Candida

High pH:

  • Bacterial vaginosis (Gardnerella, mobiluncus)
  • Trichomonas
156
Q

mechanism of PTU

Clinical use

SE

A

inhibits both peroxidase and 5’ deiodinase

Preferred for pregnant women in first trimester

SE: Agranulocytosis, liver dysfunction

157
Q

mechanism of Methimazole

Clinical use

SE

A

inhibits peroxidase only (not 5’-deiodinase)

Preferred in general (and 2/3rd trimester in preg)

SE: Agranulocytosis, fetal aplasia cutis (Scalp defect)

158
Q

function of thyroid hormone

A

Bone growth (synergism with GH)

Increase Beta 1 receptors in heart

Increase BMR (via increase Na/K ATPase activity)

Glycogenolysis/gluconeogenesis/lipolysis

159
Q

What is Graves’ disease associated with

A

HLA-DR3 and HLA-B8

4:1 female predominance

160
Q

Toxic multinodular goiter, what is it, MOA

A

Focal patches of hyperfunctioning follicular cells working independently of TSH due to mutation in TSH receptor

161
Q

Jod-Basedow phenomenon

A

Tyrotoxicosis if a pt with iodine deficiency goiter is made iodine replete

162
Q

Subacute thyroiditis (de Quervain)

Findings

Associated with?

A

self limited hypothyroidism often following a flu-like illness. May be hyperthyroid early in course

Findings:
increased ESR, jaw pain, early inflammation, very tender thyroid (Quervain is assoc with pain)

Assoc:
HLA-B35, with female predominance
Viral infections

163
Q

Treatment of thyroid storm

A

Beta blocker
PTU or methimazole
Prednisolone

164
Q

what is hashimotos assoc with

A

HLA-DR5 and HLA-B5

165
Q

Most common cause of hypothyroidism

A

Hashimotos thyroiditis (autimmune, antithyroid peroxidase, anitthyroglobulin antibodies)

166
Q

Risk of hashimotos

A

increased risk of non hodgkin lymphoma

167
Q

Presentation of hashimoto thyroiditis

A

may be euthyroid or hyperthyroid early in course due to thyrotoxicosis during follicular rupture

Histo: Hurthle cells, lymphoid aggregate with germinal centers

Moderately enlarged nontender thyroid

168
Q

subacute thyroiditis (de quervain) vs. hashimoto thyroiditis

A

Subacute thyroiditis is granulomatous infiltration vs. Hashomoto’s lymphocytic inflammation

Subacute is PAINFUL goiter, hashmoto is PAINLESS goiter

169
Q

Riedel’s thyroiditis
how does it present

histo?

complication?

proposed mechanism?

A

fixed, hard, rock-like painless goiter. Similar to Undifferentiated/anaplastic carcinoma (but that is seen in older people)

HIsto:
Fibrosis
macrophages
Eosinophils

complicated by fibrosis extending to local structures (airway) mimicking anaplastif carcinoma

IgG4-related systemic disease

170
Q

medical causes of hypothyroidism

A
  • Amiodarone
  • Tyrosine kinase inhibitors
  • Lithium
171
Q

what types of thyroid cancer are there

A 
papillary carcinoma
follicular carcinoma
medullary carcinoma
undifferentiated/anaplastic carcinoma
lymphoma
172
Q

Papillary carcinoma of thyroid
occurence/prognosis

Histo findings?

Risk factors?

A

Most common, with excellent prognosis

Empty appearing nuclei (Orphan annie eyes), Psamomma bodies, nuclear grooves,

increased risk with:
RET and BRAF mutations, or NTRK1,
Radiation and Tobacco

[activation of tyrosine kinase receptor]

173
Q

Follicular carcinoma of thyroid
Occurance/prognosis

Histo

Complication

risk factors

A

2nd most common, prognosis okay

uniform cuboidal cells lining follicles, invades thyroid capsule (unlike follicular adenoma),

Can spread hematogenously

Risk:

  • RAS mutation
  • PAX8-PPAR gamma1 rearrangement
174
Q

Medullary carcinoma of thyroid

Histo?

Association?

Tx?

A

From parafollicular C cells, produces calcitonin

Sheets of cells in an amyloid stroma

Assoc with MEN2A and MEN2B (RET mutations)

[activation of tyrosine kinase receptor]

Tx: No response to radioactive treatment, so only surgery

175
Q

Undifferentiated/anaplastic carcinoma of thyroid

A

Poor prognosis, found in older patients. Similar to Riedel ( except that is in younger pt.)

Invades local structures

176
Q

Lymphoma of thyroid

A

assoc w/ hashmoto thyroiditis

177
Q

Surgical complications for thyroid removal

A

Parathyroid damage/removal
-Hypocalcemia

Dmg to recurrent laryngeal nerves
-hoarseness

178
Q

What rises in hypothyroidism

A

LDL

Total cholesterol

179
Q

What are the causes of hypertrophic cardiomyopathy

A

most familial autosomal dominant (beta-myosin heavy-chain mutation)

Friedreich ataxia

180
Q

Causes for dilated cardiomyopathy

A 
ABCCCD
alcohol abuse
wet Berberi
Coxsackie B virus myocarditis
Cocaine use
Chagas disease
Doxorubicin toxicity
Hemochromatosis and peripartum cardiomyopathy
181
Q

causes of restrictive cardiomyopathy

A

Sarcoidosis
Amyloidosis
Postradiation fibrosis
Endocardial fibroelastosis (thick fibroelastic tissue in endocardium of young children)
Loffler syndrome (endomyocardial fibrosis with prominent eosinophilic infiltrate)
Hemochromatosis (dilated cardiomyopathy may also occur)

182
Q

What is the biochemical pathway of sorbitol?

A

Glucose to Sorbitol to Fructose

Enzymes are
Aldose reductase
Sorbitol dehydrogenase

183
Q

What tissues have aldose reductase but do not have sorbitol dehydrogenase (leading to sorbitol trapping)

A

Schwann cells
Lens
Retina
Kidney

184
Q

Diabetic ketoacidosis vs. HHS

A

DKA:

  • Ketosis
  • No serum hyperosmolarity
  • Hyperglycemia (>300)

HHS:

  • No ketosis
  • Serum hyperosmolarity
  • Extreme hyperglycemia (>800)
185
Q

for Type II diabetes, what are the drug medication classes useful

A 
Biguanides
Sulfonylureas
Thiazolidinediones
DPP-4 inhibitors
GLP-1 agonists
Others
186
Q

Biguanides (Metformin)

Other uses

Effects

SE

A

Effective, low risk for hypoglycemia, no wt gain, low cost, few SE. can be used in patients without pancreatic fxn.

Other uses:
prediabetes and PCOS

Effects:

  • Decrease gluconeogenesis in the liver
  • Decrease LDL
  • Decrease triglycerides
  • increase glycolysis
  • increase peripheral glucose uptake (insulin sensitivity)

SE:

  • GI upset
  • Lactic acidosis (CI in renal failure)
187
Q

Sulfonylureas
Mech

Examples

SE

A

Close K+ channel in beta-cell membrane so cell depolarizes resulting in insulin release. REQUIRES PANCREATIC FXN

Glimepriride/Glipizide/Glyburide (more problems with hypoglycemia, so not used much)

SE: Hypoglycemia and wt gain

188
Q

Thiazolidinediones action

mechanism, resulting in…

SE

Risks

A

increased sensitivity to insulin in the peripheral tissue

Mech: binds to PPAR-gamma receptor, results in

  • regulates fatty acid storage
  • regulates glucose metabolism

SE:

  • Weight gain,
  • Edema,
  • Hepatotoxicity,
  • Heart failure

Risks:

  • Risk of MI (Rosglitazone)
  • Risk of bladder cancer and osteoporosis (Pioglitazone)
189
Q

DPP-4 inhibitors
Examples

General description

Mech

A

Sitagliptin/Alogliptin/Saxagliptin/Linagliptin

Low risk of SE, hypoglycemia, and is wt neutral. But not as effective.

Prevent’s DPP-4s inactivation of GLP-1

190
Q

GLP-1 analogs examples

Mech

SE:

CI:

A

Exenatide/Liraglutide

Mimic incretins, decreasing glucagon secretion and increasing insulin secretion, delayed gastric emptying

SE: increased risk for acute pancreatitis, nausea

CI: insulin use

191
Q

Amylin analogs examples

Mech

Use

SE

A

Pramlintide

Decreases glucagon secretion and gastric emptying

USE: only in patients taking insulin, but either Type 1 and Type 2 DM

SE: hypoglycemia, nausea, diarrhea

192
Q

alpha-glucosidase inhibitors
examples

Mech

SE:

A

Acarbose/Miglitol

Inhibits intestinal brush border alpha glucosidases–>delayed sugar hydrolysis and glucose absorption leading to decrease in postprandial hyperglycemia

SE: GI disturbances

193
Q

standard Treatment for DKA

A

IV fluids
IV insulin
Potassium replacement

194
Q

standard Treatment for DM type I

A

Insulin

195
Q

standard Treatment for DM type II

A

Low carb diet, wt loss, oral hypoglycemic agents, insulin

196
Q

type 2 dm drug with lactic acidosis as rare but worrisome side effect

A

Metformin

197
Q

type 2 dm drug with hypoglycemia as most common SE

A

Sulfonylureas

198
Q

type 2 dm drug with recommended first line treatment for most patients

A

Metformin

199
Q

type 2 dm drug with Not safe in settings of hepatic dysfunction or CHF

A

TZD (Thiazolidinediones)

200
Q

type 2 dm drug with should not be used in patients with elevated serum creatinine

A

Metformin

201
Q

type 2 dm drug with Should not be used in pt with cirrhosis or inflammatory bowel disease

A

alpha-glucosidase inhibitors

202
Q

type 2 dm drug with not associated with wt gain

A

Metformin

203
Q

type 2 dm drug with metabolized by liver, excellent choice in pt with renal disase

A

TZDs

204
Q

type 2 dm drug with MOA closing potassium channel on beta cells, epolarization, ca influx, insulin release

A

Sulfonylureas

205
Q

type 2 dm drug with MOA inhibits alphaglucosidase at intestinal brush border

A

Alphaglucosidase inhibitors (acarbose/Miglitol)

206
Q

type 2 dm drug with MOA agonist at PPARgamma receptors leading to improved target cell response to insulin

A

TZDs

207
Q

type 2 dm drug with MOA decreasing hepatic gluconeogenesis

A

Metformin

208
Q

type 2 dm drug with good for wt loss

A

GLP-agonists

209
Q

type 2 dm drug with Avoid in hypoglycemia

A

sulfonylureas

210
Q

type 2 dm drug with Best treatment for anyone with organ failure

A

Insulin

211
Q

Pt with normally well controlled type I diabetes but gets DKA. what is the diff dx?

A 
infection
dehydration
nonadherence to insulin
severe medical illness (MI or trauma)
steroids
alcohol or drug abuse
212
Q

Leptin action

A

Inhibits Lateral hypothalamus
Stimulates ventromedial nuclei

Both reslut in satiety

213
Q

What is seen in kwashiokor

A

skin lesions
edema
liver function

214
Q

what is seen in marasmus

A

tissue and muscle wasting

loss of subcutaneous fat

215
Q

what vitamins should vegetarians supplement in their diet

A

vitamin B12

216
Q

Anti-GBM antibodies (IF)

A

Goodpasture syndrome

217
Q

Kimmelstiel-Wilson lesions

A

Diabetic nephropathy

218
Q

Spike and dome appearance

A

Membranous glomerulonephritis

219
Q

Tram track appearance of subendothelial humps

A

Membranoproliferative glomerulonephritis

220
Q

subepithelial humps

A

Acute poststreptococcal glomerulonephritis

221
Q

RLE of heme synthesis and its required cofactor

A

aminolevulinic acid synthase

Vit B6 is required cofactor

222
Q

What makes aminolevulinic aci

A

glycine and succinyl CoA

223
Q

Acute intermittent porphyria, what causes it

how does it present

tx

A

deficiency in porphobilinogen deaminase (uruporphyrinogen 1 synthase)

presents as the 5 P’s

  • painful abdomen
  • port wine urine
  • polyneuropathy
  • psychological disturbances
  • precipitated by drugs (barbiturates, seizure drugs, rifampin, metoclopramide)

tx: glucose and heme, which inhibits the ALA synthase

224
Q

Porphyria cutanea tarda

cause

presentation

associations

A

most common form of porphyria

deficiency in uroporphyrinogen decarboxylase

presents:

  • blistering of the skin
  • tea colored urine
  • hypertrichosis
  • facial hyperpigmentation

assoc with:
Hepatitis C
Alcoholism
Elevations of your LFTs

225
Q

How does lead poisoning effect heme synthesis?

presentation

Tx

A
  • ALA dehydratase
  • Ferrochelatase (leading to increased levels of protoporphyrin in RBC)

presents:
microcytic anemia, GI and kidney disease
Children:exposure to lead paint leading to mental deterioration
Adult: environmental exposure leading to headache/memory loss/deyelination
Encephalopathy/Memory loss and delirium and mental deterioration/Foot drop or wrist drop
lead lines in gingevae (burton lines)
sideroblastic anemia in BM
Basophilic stippling in RBC
abdominal colic
renal failure

tx:
EDTA or succimer in either kids or adults
Dimercaprol and succimer for severe in kids

226
Q

What tumors can increase EPO?

A

Potentially Really High Hematocrit

Pheochromocytoma
Renal cell carcinoma
Hepatocellular carcinoma
Hemangioblastoma

*trisomy 21 at birth

227
Q

Where does fetal erythropoesis occur?

A

yolk sac 3-8 wks
liver and spleen
bone marrow after 28 weeks

228
Q

in which adult bones does erythropoiesis take place?

A

Vertebrae, ribs, pelvis

229
Q

what substrate and cofactor for generating GABA

A

Glutamate and B6

230
Q

what can iron deficiency manifest as

A

Plummer-Vinson syndrome:
Iron deficiency anemia
Esophageal webs
Atrophic glossitis

231
Q

how do you distinguish folate from B12 deficiency in megaloblastic anemia

A

B12 has neurologic deficits (peripheral neuropathy/dementia)

Folate deficiency, MethylMalonicAcid will be normal (b12 will be increased)

232
Q

Causes of macrocytic nonmegaloblastic anemia

A 
Liver disease
Alcoholism
Reticulocytosis leading to increased MCV
Drugs:
-5-FU
-Zidovudine
-Hydroxyurea
233
Q

Causes of normocytic nonhemolytic anemia

A

Anemia of chronic diseas e(can go to microcytic)
Aplastic anemia
CKD

234
Q

women develops intense muscle cramps and darkening of her urine after exercise.

A

McArdle disease

235
Q

Immune thrombocytopenia (ITP)

A

antibodies bind to 2b/3a on the surface of platets–>immune system removes and destroys those platelets

Plateet count is low

Increased megakaryocytes on BM biopsy

tx:Steroids, IVIG, Splenectomy

236
Q

Thrombotic thrombocytopenic purpura (TTP)

A

Widespread platelet thrombosis, thrombocytopenia because used up

Bleeding and purpura

Deficiency in metalloprotease ADAMTs13, normally cleaves vWF multimers into smaller active vWF units.excessive platelet activation and aggregation.

237
Q

HUS-hemolytic uremic syndrome

associated with

A

classic triad, milder form of TTP

  • hemolysis
  • renal insufficiency
  • thrombocytopenia

associated with E. coli 0157:H7 infectino

238
Q

TTP pentad

A

FAT RN
or
Nasty Fever Torched His Kidneys

  • hemolysis
  • renal insufficiency
  • thrombocytopenia
  • neurological symptoms
  • fever
239
Q

von Willebrand disease

tx:

A

defect of vWF so…

  • Increase in PTT (normally stabilizes and protects factor VIII)
  • Prolonged bleeding time (Binds to subendothelial collagen and to glcyoprotein 1b)

tx:
DDAVP, desmopressin, which increases the release of vWF from endothelial cells

240
Q

DIC, disseminated intravascular coagulation

A

Widespread activation of clotting, consuming all platelets and coagulation factor

results

  • prolonged bleeding time
  • increased PT and PTT
  • low fibrinogen
  • High D-dimer (fibrin split products)
  • Schistocytes
  • Bleeding
  • Multi-organ failure
241
Q

DIC causes

A

STOP Making Thrombi

Sepsis
Trauma
Obstetric complications
Acute Pancreatitis
Malignancy
Transfusion
242
Q

fructose intolerance enzyme deficiency

A

aldolase b

243
Q

essential fructosuria enzyme deficiency

A

fructokinase

244
Q

classic galactosemia deficiency

A

galactose-1-phosphate uridyltransferase

245
Q

Wiskott Aldrich

A

WAITER

  • Wiskott
  • Aldrich
  • Immunodeficiency
  • Thrombocytopenia and purpura
  • Eczema
  • Recurrent pyogenic infections
246
Q

Hemosidinuria and thrombosis

A

PNH, paroxysmal nocturnal hemoglobinuria

247
Q

Leukemia vs. lymphoma

A

Leukemia is in bone marrow or may spill into peripheral blood

Lymphoma is in lymph node

248
Q

what is Marginal cell MALToma associated with

A

Sjogren syndrome
Hashimoto thyroiditis
H. pylori

249
Q

most common type of non Hodgkin lymphoma in adults?

In children

A

adults: diffuse large B cell lymphoma

Children: lymphoblastic lymphoma

250
Q

How does multiple myeloma present

A

anemia
renal insufficiency
back pain
hypercalcemia

251
Q

Most common leukemia in children

A

ALL

252
Q

most common leukemia in adults in US

A

CLL

253
Q

Myelodysplastic syndromes have a tendence to progress to

A

AML

254
Q

Myeloproliferative disorders may progress to

A

AML

255
Q

Numerous basophils, splenomegaly, negative for leukocyte alkaline phosphatase (LAP)

A

CML

Step 1 Journal RC (9 decks)

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