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DIT Flashcards

1
Q

Kluver Bucy Syndrome clinical features and cause?

A 
Disinhibited
Hyperdocility
Hyperorality
Hypersexuality
Curiosity

Caused by bilateral amygdala lesions

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2
Q

Order of human needs as described by Maslow

A 
Self actualization
Esteem
Love and belonging
Safety
Physiological
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3
Q

Erikson’s stages of development: infant

A

Basic trust vs. mistrust

birth-18 months

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4
Q

Erikson’s: Toddler

A

Autonomy vs. shame

18 months-3 years

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5
Q

Erikson’s preschooler

A

Iniitiative vs. guilt

3 years-5 years

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6
Q

Erikson’s school-age child

A

Industry vs. inferiority

6-12 years

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7
Q

Erikson’s adolescent

A

Identity vs. role confusion

12-18 years

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8
Q

Erikson’s young adult

A

Intimacy vs. isolation

18-35 years

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9
Q

Erikson’s Middle aged adult

A

Generativity vs. self absorption

35-55 years

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10
Q

Older adult

A

Integrity vs. despair

55 years to death

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11
Q

What structural motifs allow for proteins to bind to dNA

A

helix loop helix
helix turn helix
zinc finger
Leucine zipper protein

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12
Q

What are the different RNA polymerases in eukaryotes?

A

RNA polymerase I: rRNA
RNA polymerase II: mRNA
RNA polymerase III: tRNA

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13
Q

Treat ADHD

A

Methylphenidate and dextroamphetamine
(CNS stimulants, cause release of catecholamines at the synaptic cleft)

or

Atomoxetine (norepinephrine reuptake inhibitor)

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14
Q

conduct disorder vs. anti-social personality disorder

A

less than 18 yo

older than 18

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15
Q

Oppositional defiant disorder vs. conduct disorder

A

Deep down they know its wrong

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16
Q

Treatment for tourette

A

behavioral therapy
fluphenazine
pimozide
tetrabenzine

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17
Q

Characteristics of autism spectrum disorder

A

Living in his own world

early childhood

lack of responsiveness to others

poor eye contact

absence of social smile

impairments in commnication

peculiar repetitive ritualistic habitis

fascination with specific seemingly mundane objects

below normal intelligence

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18
Q

Rett disorder

A

similar presentation to autism spectrum disorder

x linked dominant, seen almost exclusively in girls (homozygous dominant die in utero)

Loss of milestones or developmental regression

Intellectual disability

Ataxia

Loss of verbal abilities

Hand wringing and hand to mouth gestures

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19
Q

Causes of transudative pleural effusion

A 
CHF
Cirrhosis
Nephrotic syndrome
Pulmonary embolus
Fluid overload
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20
Q

How is emphysema from smoking different than alpha1-antitrypsin deficiency

A

Smoking-centriacinar

alpha1-antitrypsin deficiency-panacinar

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21
Q

Treatment of anorexia

A

Psychotherapy, nutrtional

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22
Q

Signs of bulimia

A

Enlarged parotid glands
Increased serum amylase
Erosion of enamel of teeth
Hypokalemic hypochloremic metabolic alkalosis

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23
Q

Hypokalemic hypochloremic metabolic alkalosis

A

Stomach puts bicarb into serum to buffer the acid reabsorption, which doesnt happen. so you get alkalotic.

Opposite to DKA, you get hypokalemic b/c the potassium goes into the cells.

Chloride follows H+

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24
Q

Treatment of bulimia

A

SSRI (fluoxetine) with psychotherapy

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25
Q

Criteria for anorexia

A
  • Distorted body image
  • Intense fear of gaining weight
  • Refusal to maintain normal body weight, with BMI
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26
Q

Criteria for binge eating disorder

A

Episodes of binging with sense of lack of control

At least 3/5

  • Eating faster
  • Eating until uncomfortably full
  • Eating large amounts when not hungry
  • Eating alone
  • Feeling badly about it

Marked distress or remorse
At least 1x/week for 3 months with no compensatory behavior

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27
Q

What are the different RNA polymerases in prokaryotes

A

Only one.

Makes 3 types of RNA

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28
Q

What enzyme is deficient in Lesch-Nyhan syndrome?

Treatment

A

HGPRT (hypoxanthine-guanine phosphoribosyltransferase)

Tx: Allopurinol [for hyperuricemia/gout but mental disorder still present]

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29
Q

Causes of an exudative pleural effusion

A 
Pneumonia
Infection
TB
Cancer
Uremia
Connective tissue disease
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30
Q

Stages of Behavioral change

A 
Precontemplation
Contemplation
Preparation/determination
Action/Willpower
Maintenance
Relapse
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31
Q

Alcohol action

A

GABA receptors (like benzodiazepine and barbiturates)

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32
Q

Alcohol withdrawal symptoms

A 
agitation
anxiety
insomnia
tremor
formication
Deliirium tremens is severe
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33
Q

Delirium tremens

A

2-3 days after cessation of alcohol (often seen in post op)

seizures and extreme autonomic hyperactivity

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34
Q

Treatment of alcohol withdrawal

A

Benzodiazepines

Alcohol

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35
Q

Screening for alcoholism

A 
CAGE
Cut back
Annoyance
Guilt
Eye-opener
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36
Q

Wernicke Korsakoff syndrome

Where does damage happen

Treatment

What to NOT DO

A

Thiamine (B1) deficiency

Wernicke encephalopathy (acute)
and
Korsakoff syndrome (long term consequence)

Damage to

  • Medial thalamus
  • Mammillary bodies of posterior hypothalamus

Tx: IV thiamine

DO NOT give glucose without thiamine first. because active thiamine is required for metabolism of glucose.

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37
Q

Wernicke encephalopathy

A 
Confusion
Nystagmus
Ophthalmoplegia
Ataxia
Sluggish pupillary reflexes
Coma and death if untreated
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38
Q

Korsakoff syndrome

A

Anterograde amnesia
Retrograde amnesia
Confabulation
Hallucinations

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39
Q

Long term treatment of alcoholism

A
  • AA: is tried and true best relapse prevention
  • Naltrexone (also opioid antagonst)
  • Disulfiram [inhibits acetylaldehyde dehydrogenase]
  • Topiramate [affects glutamate receptors, also used for migraine prevention and seizures]
  • Acamprosate (campral) [also affects glutamate receptors]
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40
Q

Time frame for schizophrenia

A

> 6 months

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41
Q

Time frame for brief psychotic episode

A
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42
Q

Time frame for schizophreniform

A

1-6months

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43
Q

Criteria for schizoaffective disorder

A

Psychotic symptoms for 2 weeks or more in absence of mood disorder

AND

A time period with BOTH psychosis and a major mood disorder episode at the same time

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44
Q

Positive symptoms of schizophrenia

Theory

A

delusions
halucinations
disorganized speech
Grossly disorganized/catatonic

Increased dopamine to mesolimbic system

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45
Q

Negative symptoms of schizophrenia

Theory

A 
alogia
avolition
affective flattening
social withdrawal
thought blocking
poor grooming

Decreased dopamine to mesocortical

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46
Q

How long does a delusional disorder last?

A

> 1 month

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47
Q

Characteristic finding for EM of dendritic cell with Langerhans cell histiocytosis

A

Birbeck granules, “Tennis rackets”

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48
Q

Low potency typical antipsychotics

A

Chlorpromazine

Thioridazine

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49
Q

SE of low potency typical antipsychotics

A 
Anticholinergic SE
Block D2 dopamine receptors 
Block muscarinic receptors
Block alpha1 receptors--> Hypotension
Block histamine receptors-->Sedation
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50
Q

High potency typical antipsychotics

A 
Haloperidol
Fluphenazine
Loxapine
Thiothixene
Trifluoperazine
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51
Q

SE of high potency typical antipsychotics

A

Fewer anticholinergic,
EPS/Tardive dyskinesia
NMS

within first several days: acute dystonia and torticollis. Treat wtih antimuscarinic or anticholinergic drug (benztropine or diphenhydramine)

within first month: parkinsonism (bradykinesia, akinesia)

within 2 months: Akathisia (restlessness

Several months-years: Tardive dyskinesia (not an EPS). lip smacking. irrev.

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52
Q

SE Atypical antipsychotics

A

Fewer EPS
Fewer anticholinergic
Weight gain

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53
Q

Atypical antipsychotics

A 
Olanzapine
Quetiapine
Risperidone
Aripiprazole
Clozapine
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54
Q

NMS symptoms

treatment

A 
Deliirium and altered mental status
Autonomic instabliity
Muscle rigidity
Myoglobinuria
Hyperpyrexia

tx: Dantrolene [also used for malignant hyperthermia]
or dopamine agonist (bromocriptine)

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55
Q

Mech of atypical antipsychotics

A

block dopamine receptors
block serotonin receptors
block alpha-receptors:hypotension
block histamine receptors:sedation and wt gain. (especially olanzapine, also diabetes)

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56
Q

Clozapine

A

Strongest most effective atypical antipsychotics

But Agranulocytosis!! so need to check CBC weekly. Ergo third line antipsychotic.

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57
Q

Quetiapine

A

treat psychosis from parkinson meds

Lowest risk of EPS

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58
Q

Mania

A

> 1 wk. distinct period of abnormally and persistently elevated, expansive or elevated mood.

SEveree enough to cause

  • marked impairment in social or occupation function
  • require hospitalization
  • psychotic features

DIGFAST

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59
Q

DIGFAST

A

MANIA

Distractibility
Irresponsibility
Grandiosity
Flight of ideas
Activity/agitation
Sleep (decreased need)
Talkativeness/pressured speech
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60
Q

Hypomania (why different than mania)

A

same symptoms but less severe

> 4 days

No marked impairment in social or occupational functioning!

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61
Q

Bipolar I disorder

Bipolar II disorder

A

1 manic episode

vs. Hypomanic episode and 1 episode of major depression

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62
Q

NT changes in Depression

A

Decreased Dopamine
Decreased Serotonin
Decreased NE

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63
Q

NT changes in Mania

A

Increased serotonin

Increased NE

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64
Q

Cyclothymic disorder

A

at least 2 years of mild hypomanic and mild depressive symptoms.

with no periods of normal mood longer than 2 months!

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65
Q

Treatment of bipolar disorder

A

Lithium

Atypical antipsychotics

  • Risperidone
  • Aripiprazole
  • Olanzapine

Antiepileptic

  • Lamotrigine
  • Valproic acid
  • Carbamazepine
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66
Q

SE of lithium

A 
sedation and dizziness
tremors
sick sinus syndrome
bradycardia
heart block
hypothyroidism
goiter
polyuria (blocking ADH action by blocking the luminal Aquaporin channels)-->Nephrogenic diabetes insipid
Ebstein anomaly
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67
Q

Ebstein anomaly

A

Tricuspid leaflets are displaced inferiorly into the right ventricle

Hypoplasia of the right ventricle

Tricuspid regurgitation or stenosis

Patent foramen ovale

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68
Q

Most common SE of lithium to occur rapidly (or any other time)

A

tremor

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69
Q

SSRI drugs

A 
Fluoxetine
Paroxetine
Sertraline
Fluvoxamine
Escitalopram
Citalopram
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70
Q

SNRI drugs

A

Venlafaxine
Duloxetine
Desvenlafaxine

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71
Q

TCAs drugs

A 
Desipramine
Nortriptyline
Imipramine
Amitriptyline
Doxepin
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72
Q

MAOI drugs

A

Tranylcypromine
Phenelzine
Isocarboxazid

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73
Q

MDD with seasonal pattern

A

> 2 years
2 major depressive episodess
2 year time frame
No non-seasonal episode of MDD during the 2 years

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74
Q

SADPERSONS

A 
Sex (males)
Age (45)
Depression
Previous attempt
Ethanol/drug use
Rational thinking (loss)
Sickness
Organized plan
No spouse/no social support
Stated future intent
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75
Q

SSRI

A

Citalopram
Fluoxetine
Paroxetine
Sertraline

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76
Q

serotonin syndorme

treatment

A 
hyperthermia
hyperreflexia/myoclonus
autonomic instability
flushing
diarrhea
MSC

Tx:

  • Cooling down
  • Benzodiazepines
  • Stopping the medications

-Cyproheptadine (serotonin antagonist, but not first line)

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77
Q

SNRIs

A

Desvenlafaxine
Venlafaxine
Duloxetine (also approved for neuropathic pain)
Milnacipran (only for fibromyalgia, not depression)

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78
Q

TCAs

A 
Amitriptyline
Nortriptyline
Imipramine
Desipramine
Clomipramine
Doxepin
Amoxapine
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79
Q

TCAs and their uses

A

Imipramine-enuresis
OCD-clomipramine
Fibromyalgia-amitriptyline
Neuropathic pain-amitriptyline

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80
Q

TCA SE

and Tx

A 
Convulsions
Coma
Cardiotoxicity
Respiratory depression
Hyperpyrexia
Confusion and hallucination

if CV toxicity–>Sodium bicarbonate (because trap the weak acid TCA in the urine and excreted)

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81
Q

MAOI

A

Tranylcypromine
Phenelzine
Isocarboxazid
Selegilene (not antidepressant, MAO-B just for dopamine for parkinsonism)

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82
Q

MAOI SE

A

Hypertensive crisis (tyramine ingestion).

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83
Q

Atypical antidepressants

A

Bupropion
Mirtazapine
Trazodone

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84
Q

Bupropion
use

mech

SE

A

Smoking cessation
antidepressant

inhibits reuptake of norepinephrine and dopamine

  • Lowers seizure threshold
  • stimulant (don’t use at night)
  • NO SEXUAL SE, so can use in lieu of SSRI
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85
Q

Mirtazapine
Mech

SE

A

alpha2 antagonist, promoting further norepinephrine release.
similar to SSRI except serotonin2 and serotonin3 receptor antagonist

SE:
-Sedation
Increased appetite
-Wt gain
-Dry mouth
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86
Q

Trazodone
Mech

Use

SE

A

inhibits serotonin reuptake

not for depression because would require too high dose. used for insomnia.

along with bupropion can be used as adjunct for SSRI or SNRI

SE:

  • Sedation
  • Priapism
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87
Q

Seronegative spondyloarthropathies

A

PAIR

Psoriatic arthritis
Ankylosing spondylitis
Inflammatory Bowel disease
Reactive arthritis (Reiter syndrome0

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88
Q

Hartnup disease

A

Deficiency of transporter for neutral AA (tryptophan)

Can't make niacin-->pellagra
Dermatitis
Diarrhea
Dementia
Death
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89
Q

Full saturation of glucose transporters

A

Begin spilling at 160

Fully saturated at 350

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90
Q

Psamomma bdoesis

A

Papillary adenocarcinoma
Serous cystadenocarcinoma of the ovary
Meningioma
Mesothelioma

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91
Q

lyti8c bone lesions on xray

A

multiple myeloma

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92
Q

What are the toxins for strep pyogenes

A

Streptolysin O-hemolysis on blod agar plates, oxygen labile

Streptolysin S-oxygen stable

Streptococcal pyrogenic exotoxins type A, B, and C- erythrogenic toxins

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93
Q

What is HUS

A

Hemolytic uremic syndrome

O157:H7 serotype E. coli

Hemolytic anemia
Thrombocytopenia
Acute renal failure

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94
Q

How are organic anions secreted in the proximal convoluted tubule?

A

Alpha ketoglutarate/Organic anion antitransporter.

Alpha ketoglutarate is brought into cell by Alpha ketoglutarate/Na+ cotransporter.

Na/K ATPase sets up gradient

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95
Q

How are organic cations secreted into the proximal convoluted tubule?

A

3Na2K ATPase, sets up electrical gradient.

Organic cation/H+ cotransporter

96
Q

What are the Tubular Fluid/Plasma concentrations of various substances along the proximal tubule?

A

PAH steepest

Creatinine and Inulin linearly up

Urea

Chloride

Potassium and sodium along the 1.0 line (slightly above , potassium slightly hgiher)

Phosphate below,

Amino acids and Glucose very much lower

97
Q

What class of drugs inhibits the Na+/2Cl-/K+ symporter int he thick ascending limb and what is the result

A

Loop diuretics, leading to isotonic H2O secretion

98
Q

Where does PTH act on the kidney?

A

Early distal tubule: increase Ca2+/Na+ exchange–>Calcium reabsorption

Early proximal convoluted tubule: Inhibits Na+/PO4 cotransport–>Phosphate excretion

99
Q

What are the 2 types of cells composing the collecting duct and the last segment of the distal tubule? What do they do?

A

Principal cells:

  • Reabsorb H2O and Na+
  • Secrete K+

Intercalated cells:

  • Secrete H+ or HCO3-
  • Reabsorb K+
100
Q

What are the two types of intercalated cells

A

Alpha cells–>Secrete H+

Beta cells–> Secrete HCO3-

101
Q

What are the potassium sparing diuretics?

A

Aldosterone antagonists

  • Spironolactone
  • Eplerenone

Inhibit epithelial Na+ channels

  • Triamterene
  • Amiloride
102
Q

What effect does aldosterone have on the principal cells and intercalated cells

A

Principal cells: reabsorption of Na+ and secretion of K+

Intercalated cells: Stimulates the secretion of H+

103
Q

What happens at the thick ascending limb?

A

H2O impermeable

Ca2+ and Mg2+ are reabsorbed

Na/2Cl/K cosymporter is inhibited by loop diuretics

104
Q

What are the uses for mannitol

A

Drug overdose, increased ICP, increased intraocular pressure (use for acute close angle glaucoma)

105
Q

What are the uses for acetazolamide

A

Chronic glaucoma, urinary alkalinization,metabolic alkalosis, altitude sickness, pseudotumor cerebri

106
Q

What are the loop diuretics

A

Furosemide
Bumetanide
Torsemide
Ethacrynic acid (not a sulfa drug)

107
Q

SE to Furosemide

A

OH DANG!

  • Ototoxicity
  • Hypokalemia
  • Dehydration
  • Allergy
  • Nephritis
  • Gout

ototoxicity and nephrotoxicity when given with aminoglycoside

108
Q

Uses for thiazides

A
  • HTN
  • Idiopathic hypercalciuria (unless serum is also high as n hyperPT)
  • Nephrogenic diabetes insipidus
109
Q

SE of thiazides

A 
Hypokalemia
Hyponatremia
Hyperglycemia
Hyperlipidemia
Hyperuricemia
Hypercalcemia

-Sulfa allergy!

110
Q

Treatment of central DI

A

Intranasal desmopressin

111
Q

Treatment of nephrogenic DI

A

Hydrochlorothiazide (increase proximal reabsorption)

Indomethacin (2nd line or adjunct), inhibit prostaglandin synthesis and decrease renal blood flow and renal output

112
Q

Treatment for nephrogenic DI lithium induced

A

Amiloride, blocks the sodium channels that lithium uses to enter the prinicpal cell

113
Q

Causes of increased anion gap metabolic acidosis

A 
MUDPILES
Methanol
Uremia
Diabetic ketoacidosis
Propylene glycol
Iron tablets or isoniazid
Lactic acidosis
Ethylene glycol 
Salicylate
114
Q

Causes of normal anion gap metabolic acidosis

A 
HARD-ASS
Hyperalimentation
Addison disaease
Renal tubular acidosis
Diarrhea
Acetazolamide
Spironolactone
Saline infusion
115
Q

what nerve runs with anterior interosseous artery

A

anterior interosseous nerve

116
Q

What nerve runs with posterior interosseous artery

A

deep branch of the radial nerve

117
Q

what nerve runs with the posterior circumflex artery

A

axillary nerve

118
Q

what nerve runs with the suprascapular artery

A

suprascapular nerve

119
Q

What nerve rusn with the thoracodorsal artery

A

thoracodorsal nerve

120
Q

what nerve runs with the deep brachial artery

A

radial nerve

121
Q

what nerve rusn with the dorsal scapular nerve

A

dorsal scapular nerve

122
Q

what nerve runs with the lateral thoracic artery

A

long thoracic nerve

123
Q

what nerve runs with the ulnar artery

A

ulnar nerve

124
Q

what nerve runs with the brachial artery

A

medial nerve

125
Q

what causes a rash on the palms and soles

A

secondary syphilis
rocky mountain spotted fever
coxsackie A virus
Kawasacki disease

126
Q

Causes of Nephritic syndorme

A
  • Acute poststreptococcal glomerulonephritis
  • Rapidly progressive glomerulonephritis
  • Berger disease (IgA glomerulonephropathy)
  • Alport syndrome
127
Q

Causes of Nephrotic syndrome

A 
Focal segmental glomerulosclerosis
Membranous nephropathy
Minimal cahnge disease
Amyloidosis
Diabetic glomerulonephropathy
128
Q

What can present as boh nephritic and nephrotic

A

Diffuse proliferative glomerulonephritis

Membranoproliferative glomerulonephritis

129
Q

What is associated with IgA nephropathy? also what is the other name for IgA nephropathy

A

aka Berger disease

Seen with Henoch-Schonlein purpura

130
Q

When does IgA nephropathy present

A

with URI or acute gastroenteritis

131
Q

What is cause for Alport syndrome

A

Mutation in type IV collagen leading to thinning and splitting of the glomerular basement membrane. Most commonly x linked

132
Q

Presentation for Alport syndrome

A

Cant See, cant Pee, cant hear high C

Glomerulonephritis
Deafness
Eye problems

133
Q

If kidneys and lungs are attacked (Hematuria/hemoptysis).. you should think of

A

Goodpasture syndrome
and
Granulomatosis with polyangiitis (Wegeners’

134
Q

What are the possible causes of Rapidly progressive (crescentic) glomerulonephritis

A

Goodpasture syndrome

Granulomatosis with polyangiitis

Microscopic polyangiitis

Lupus

135
Q

What is notable about minimal change disease?

What causes it.

Treatment.

A

Effacement of foot processeses

Most common cause of nephrotic syndrome in children, triggered by infxns or immunizations

Tx: Corticosteroids

136
Q

causes of membrano-proliferative glomerulonephritis

A

Hepatitis b
Hepatitis C
Lupus
Subacute bacterial endocarditis

137
Q

sign of membrano-proliferative glomerulonephritis

A

Tramtrack appearance of GBM splitting caused by mesangial ingrowth

Subendothelial immune complex deposits with granular IF

138
Q

sign of membranous nephropathy

A

Spike and dome appearance with subepithelial deposits

139
Q

signs of diabetic glomerulonephropathy

A

eosinophilic round acellular nodules within the glomeruli (Kimmelstiel noduels)

Nonenzymatic glycosylation of GBM, increased permeability and thickening

Nonenzymatic glycosylation of efferent arterioles, increased GFR, mesangial expansion

140
Q

Linear pattern of IgG deposition on IF

A

Goodpasture syndrome

141
Q

Lumpy bumpy deposits of IgG, IgM, and C3 in the mesangium

A

Poststreptococcal glomerulonephritis

142
Q

Deposits of IgA in the mesangium

A

IgA nephropathy

143
Q

Anti-GBM antibodies, hematuria, hemoptysis

A

Goodpasture syndrome

144
Q

Nephritis, deafness, cataracts

A

Alport syndrome (xlinked mutation in type IV collagen)

145
Q

Crescent formation in the glomeruli

A

rapidly progressive glomerulonephritis

146
Q

Wire-loop appearance on LM

A

Diffuse proliferative glomerulonephritis

147
Q

Nephrotic syndrome associated with HIV

A

focal segmental glomerulosclerosis

148
Q

Nephrotic syndrome associated with Hep B

A

Membranoproliferative glomerulonephritis

149
Q

EM:spiking of the GBM due to subendothelial depostis

A

Membranous nephropathy

150
Q

nodular hyaline deposits in the glomeruli

A

Kimmelstiel wilson onodules (diabetic nephropathy)

151
Q

Glomerulonephritis plus pulmonary vasculitis

A

Granulomatosis with polyangiitis

Goodpasture syndrome

152
Q

What nerve most likely damaged in fibular neck fracture

A

deep peroneal nerve

153
Q

RBC cast

A

glomerular damage

154
Q

WBC cast

A

acute pyelonephritis

155
Q

Bacterial cast

A

pyelonephritis

156
Q

Epithelial cell cast

A

ATN (acute tubular necrosis), toxic ingestions

157
Q

Waxy cast

A

Chronic renal failure

158
Q

Hyaline cast

A

nonspecific, can be normal, often in concentrated urine samples

159
Q

Fatty cast

A

nephrotic syndrome

160
Q

Granular cast

A

ATN, acute tubular necrosis, chronic renal disease

161
Q

What are the different types of kidney stones in order of occureance

A

Calcium (80%) (oxalate or phosphate or both)
Ammonium magnesium phosphate (15%)
Uric acid (5%)
Cystine (1%)

162
Q

which kidney stone type is radiolucent (not seen on xray). but seen on CT or ultra sound

163
Q

Calcium kidney stones treatment

causes

A

thiazides and citrate

hypercalciuria

  • cancer
  • increase pth
  • ethylene glycol (calcium oxalate)
  • increased vitamin c (Calcium oxalate)
164
Q

ammonium magnesium phosphate causes

how can it present

tx

A

urease positive bugs (proteus mirabilis, staphylococcus, klebisella) that hydrolyze urea to ammonia leading to urine alkalinization.

can present as staghorn calculi

tx: eradiction of underlying infxn and surgical removal of stone

165
Q

Cystine stone presentation and treatment

A

Can form staghorn calculi

tx: alkalinize urine

166
Q

Wilms tumor

A

most common renal malignancy of children 2-4 yo

Hematuria, large flank mass

Deletion of WT1 or WT2 on chr 11

assoc with WAGR complex

167
Q

WAGR complex

A

Wilms tumor
Anidiridia (lack of iris)
Genitourinary malformation
Retardation

168
Q

Transitional cell carcinoma

A

most common tumor of urinary tract system (can occur in renal calycyes, renal pelvis, ureters, bladder)

Painless hematuria (no casts) suggests bladder cancer

Risks:

  • Phenacetin
  • smoking
  • Aniline dyes
  • Cyclophosphamide
169
Q

drug induced acute interstitial nephritis features

A

fever
rash
eosinophilia
azotemia

170
Q

thyroid like appearance of kidney

A

chronic pyelonephritis

171
Q

Cholinesterase inhibitor poisoning presentation

A

DUMBBELSS

Diarrhea
Urinatin
Miosis
Bronchospasm
Bradycardia
Excitation
Lacrimation
Sweating
Salivation
172
Q

Blocking parasympathetic presentation

A

DUMBBeLSS (skeletal muscle and CNS excitation are mediated by nicotinic receptors)

Hot as a hare
Dry as a bone
Red as a beet
Blind as a bat
Mad as a hatter
173
Q

1st aortic arch forms what

A

Part of maxillary artery (Branch of external carotid)

[1st arch is maximal]

174
Q

2nd aortic arch forms what

A

Stapedial artery and hyoid artery

175
Q

3rd aortic arch forms what

A

Common carotid artery and proximal part of internal carotid artery

176
Q

4th aortic arch forms what

A

On left, aortic arch; on right, proximal part of right subclavian artery

177
Q

6th aortic arch forms what

A

Proximal part of pulmonary arteries and (on left only) ductus arteriosus)

178
Q

Branchial clefts derived from what

A

derived from ectoderm

aka branchial grooves

179
Q

Branchial arches derived from what

A

derived from mesoderm (muscles, arteries) and neural crest (bones, cartilage)

180
Q

Branchial pouches derived from what

A

derived from endoderm

181
Q

Branchial cleft derivatives

A

1st cleft–>external auditory meatus

2-4 clefts form temporary cervical sinuses obliterated by proliferation of 2nd arch mesenchyme

182
Q

1st branchial arch

A

Cartilage
-Meckel cartilage: Mandible, Malleus, incus, spheno-Mandibular ligament

Muscles
-Muscles of Mastication (temporalis, masseter, laterla and medial pterygoids), mylohyoid, anterior belly of digastric tensor tympany, tensor veli palitini)

Nerves
-CN V2, and V3 (chew)

183
Q

Abnormality in 1st branchial arch

A

Treacher Collins syndrome (mandibular hypoplasia, facial abnormalities)

184
Q

2nd branchial arch

A

Cartilage
-Stapes, styloid process, lesser horn of hyoid, stylohyoid ligament

Muscles
-Muscles of facial expression (Stapedius, Stylohyoid, platySma, belly of digastric)

Nerves
-CN VII (facial expression, smile)

185
Q

abnormality in 2nd branchial arch

A

Congenital pharyngocutaneous fistula (persistence of cleft and pouch–>fistula between tonsillar area and lateral neck)

186
Q

3rd branchial arch

A

Cartilage
-Greater horn of hyoid

Muscles
Stylopharyngeus, innerv by the glossopharyngeal nerve

Nerves
CN IX (stylopharyngeus) swallow stylishly
187
Q

4-6th branchial arches

A

Cartilage

  • Thyroid
  • cricoid
  • arytenoids
  • corniculate
  • cuneiform

Muscles
4th: most pharyngeal constrictors, cricothyroid, levator veli palitini

6th: all intrinsic muscles of larynx except cricothyroid

Nerves
4th: -CN X (superior laryngeal branch), simply swallow

6th: -CN X (recurrent laryngeal pbranch) [speak]

188
Q

clinical consequence of a glycolytic enzyme deficiency

A

Hemolytic anemia (no ATP for Na/K ATPase resulting in RBC swelling and lysis)

189
Q

Rate limiting step in glycolytic pathway

A

phosphofructokinase-1

190
Q

How does insulin or glucagon control glycolytic pathway

A

Glucagon receptor, Adenyl cyclase, PKA, then the phosphorylation of the PFK-2/FBP-2 complex causes FBP-2 action

results in decreased Fructose-2,6 bisphosphate

Conversely, increased insulin to glucagon ratio decreases AC, decreases PKA, hypophosphorylates the enzyme complex resulting in greater PFK-2,

results in increased Fructose-2,6 bisphosphate, resluting in sitimulated PFK-1 to go through glycolytic pathway

191
Q

what part of basal ganglia if lesioned causes hemiballismus and how

A

subthalamic nucleus lesioned in a lacunar stroke.

192
Q

Open angle glaucoma presentation

Risk factor

A

Risk factor:
>40,
black,
diabetes

Common, insidious form, bilateral

early: asymptomatic
late: areas of reduced/absent vision; contraction of visual field (peripheral to central)

193
Q

acute angle closure glaucoma

A

emergency
abrupt onset of pain, nausea, colored halos, rainbows around light

red teary eye with hazy cornea and fixed, mid dilated pupil (not reactive to light), that is firm to palpation

194
Q

What are the retroperitoneal abdominal structures

A

SAD PUCKER
A DUCK PAIR

Adrenal glands
Duodenum (2,3,4 parts)
Ureters
Colon (descending and ascending)
Kidneys
Pancreas (not tail)
Esophagus (south of diaphragm)
Aorta
Rectum
195
Q

Gluconeogenesis enzymes

A
  1. Pyruvate carboxylase (with biotin)
  2. PEP carboxykinase
  3. Fructose-1,6-bisphosphatase
  4. Glucose-6-phosphatase
196
Q

where can gluconeogenesis take place?

A

Hepatocytes
Kidney
Intestinal epithelium

197
Q

Gibbs free energy equation

A

deltaG=deltaH-T*deltaS

H=energy/enthalpy (heat change in constant pressure rxns)

S=entropy/disorder/randomness

198
Q

pathway of aqueous humor

A

ciliary body production
posterior chamber
anterior chamber,
reabsorbed by canal of schlemm

199
Q

metoclopramide mechanism

A

antagonist at the dopamine D2 receptor
Serotonin agonist

increases contractility in the GI tract

200
Q

What are the 2 functions of debranching enzyme

A

transferase 4-alpha-D-glucanotrasnferase (brings 3 of the 4 to the end of the other strand)

alpha-1,6 glucosidase (cleaves off remaining as glucose)

201
Q

What are the glycogen storage diseases and their mechanism?

A
  • McArdle (deficiency in glycogen phosphorylase) aka Glycogen storage disease type V
  • Von Gierke disease (deficiency in glucose-6-phosphatase) aka Glycogen storage disease type I
  • Cori’s disease (deficiency in alpha-1,6-glucosidase) aka Glycogen storage disease type III
  • Pompe disease (deficiency of alpha-1,4 glucosidase in the lysosomes) aka Glycogen storage disease type II
202
Q

McArdle disease (type V)

Mech

presentation

life expectancy

A

Mech: (glycogen buildup–>osmotic, lyse)

Rhabdomyolysis
-Myoglobinuria
-Renal failure
Muscle cramping

Normal life expectancy

203
Q

Von Gierke disease (Type I)

mech

presentation

treatment

A

Mech: (liver, enterocytes, kidney) cannot share glucose

Severe fasting hypoglycemia
Hepatomegaly
Enlargement of the kidneys
Elevated serum lactate
Elevated uric acid
Hypertriglyceridemia

tx: feed patient frequently, overnight give cornstarch

204
Q

Cori disease (Type III)

mech

presentation

A

Mech: (defect in debranching enzyme. cannot break alpha1,6 linkages). like milder von gierke

milder hypoglycemia
no elevation in lactate levels
no elevation in uric acid

205
Q

Pompe disease (Type II)

Mech

Presentation

A

Mech: (Deficiency of alpha-1,4 glucosidase in the lysosomes)

2 forms:

  • Infantile form
  • severe muscle weakness
  • cardiomegaly and heart failure
  • shortened life expectancy
  • Adult form, some activity but less than normal
  • No cardiac involvement
  • Gradual onset of skeletal muscle weakness
  • Diaphragm weakness
  • Respiratory failure
206
Q 
Limiting rate enzyme for
De novo pyrimidine synthesis
De novo purine synthesis
Glycolysis
Gluconeogenesis
Glycogne synthesis
Glycogenolysis
TCA cycle
Hexose monophosphate shunt
A 
Carbamoyl phosphate synthetase-2
Glutamine PRPP amidotransferase
Phosphofructokinase-1
Fructose-1,6-bisphosphatase
Glycogen synthase
glycogen phosphorylase
isocitrate dehydrogenase
Glucose-6-phosphate dehydrogenase
207
Q

what enzyme catalyzes the rate limiting step in carbohydrate digestion

A

oligosaccharide hydrolases at brush border

208
Q

what enzymes are involved in the TCA cycle that we should know

A

Citrate synthase
Isocitrate dehydrogenase (RLS)
alpha-Ketoglutarate dehydrogenase (TLC For Nobody cofactors same as PDH)

209
Q

What cofactors are needed for pyruvate dehydrogenase

A

TLC For Nobody
(same as for alpha-ketoglutarate dehydrogenase)

Thiamine (B1)
Lipoic acid
Coenzyme A (B5)
FAD (B2)
Niacin (B3)
210
Q

Uncoupling agents

A

Thermogenin
Aspirin
2,4-DNP (dinitrophenol)

211
Q

Disruptions in mitochondrial electron transport

A 
Complex 1 (NADH reductase): Amytal/Rotenone/MPP
Complex III (Cytochrome b+c1): Antimycin A
Complex IV (Cytochrome a+a3): CN/N3-/CO/H2S
H+ATPase: Oligomycin A
212
Q

What are the nitrogen carriers in the blood

A

alanine and glutamine

213
Q

required cofactor of all aminotransferases

A

Pyridoxal phosphate (deriv of vitamin B6)

214
Q

what are the 2 most important aminotransferases and what do they catalyze

A
  • Alanine aminotransferase (alanine and alpha-ketoglutarate goes to glutamate and pyruvate)
  • Aspartate aminotransferase (glutamate and oxaloacetate goes to alpha-ketoglutarate and aspartate)
215
Q

causes of acute pancreatitis

A 
BAD HITS
biliary causes
alcohol
Drugs
hypertriglyceridemia/hypercalcemia
idiopathic
trauma (ERCP)
scorpion sting
216
Q

enzymes for red cells to detoxify hydrogen peroxide

A

Glutathione peroxidase
Glutathione reductase
Glucose-6-phosphate dehydrogenase

217
Q

enzymes for production of ROS

A

NADPH oxidase
Superoxide dismutase
Myeloperoxidase

218
Q

oxidative substances

A 
Anti-malarial drugs (primaquine and chloroquine)
Nitrofurantoin
Dapsone
Sulfonamides
Isoniazid
Naphthalene
Fava beans
Ibuprofen
High dose ASA (Aspirin)
219
Q

Glucose-6-phosphate dehydrogenase deficiency presentation

A

Hemolytic anemia
Heinz bodies
Bite cells

220
Q

Prophylaxis for all malaria species except P. falciparum

A

Chloroquine

safe during pregnancy also

221
Q

Prophylaxis for resistant strais of P. falciparum

A

Atovaquone-proguanil recommended

Mefloquine is alternative drug

222
Q

Tx for P.vivax/ovale

A

Chloroquine plus primaquine

223
Q

Tx for P. falciparum

A

Chloroquine sensitive: Chloroquine without primaquine

Chloroquine resistant: quinine sulfate and doxycycline

224
Q

Essential fructosuria cause

presentation

A

Deficiency in Fructokinase

builds up in blood and spills into urine. BENIGN. just can’t use fructose as a energy source

225
Q

Fructose intolerance

Mech

Presentation

Tx:

A

Deficiency in Aldolase B. Buildup of Fructose 1-P, end up inhibiting glycogenolysis and gluconeogenesis. cannot correct fasting hypoglycemia.

Hypglycemia and vomiting (esp after consuming fructose or sucrose)

Tx: decrease intake of fructose and sucrose

226
Q

Galactokinase deficiency mechanism

presentation

A

lack of galactokinase. accumulation of galactitol (accumulates in blood and urine)–>cataracts

227
Q

Classic galactosemia mech

presentation

Treatment

A

deficiency of Galactose-1-phosphate-uridyltransferase

hepatomegaly, jaundice, failure to thrive, intellectual disability

tx: exclude lactose and galactose

228
Q

Lactase deficiency

A

lactose passes into the colon, bacteria consume.

  • gas
  • bloating, cramping, flatulence
  • osmotic diarrhea

tx: supplement lactase in diet
avoid dairy products

229
Q

rate limiting step ofpentose phosphate pathway

230
Q

what tissues use the pentose phosphate pathway

A

RBC
liver
Adrenal cortex
Mammary glands

(reducing reactive oxygen species, and for making cholesterol and fatty acids)

231
Q

tx iron overdose

A

Dferoxamine

232
Q

tx Mercury, Gold, Arsenic

A

Dimercaprol (BAL)

233
Q

tx Acetaminophen overdose

A

N-acetylcysteine

234
Q

tx: copper overdose

A

penicillamine

235
Q

tx: lead posoning

A

EDTA (Ethylenediamine tetraacetic acid)
or
Succimer

236
Q

Associations with primary biliary cirrhosis

A

Can have IBS (like UC)

Cholangiocarcinoma
Gallbladder carcinoma
Colorectal carcinoma (huge risk when you have BOTH PSC AND UC)

Step 1 Journal RC (9 decks)

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