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First Pass Miss Step 1 > The Final Pass > Flashcards

The Final Pass Flashcards

1
Q

Origin, insertion, innervation, and action of rhomboid minor?

A

Origin: Spinous processes of C7/T1
Insertion: Superior medial border of scapula
Innervation: Dorsal scapular nerve (root of C5)
Action: Retracts, elevates, and rotates scapula

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2
Q

Origin, insertion, innervation, and action of teres minor?

A

Origin: lateral scapular border superior to teres major
Insertion: Inferior facet of greater tubercle
Innervation: Axillary nerve (C5, C6) (along with deltoid)
Action: Chief external rotator of arm at 90 degrees abduction.

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3
Q

What muscles does the median nerve innervate distal to the wrist?

A

LOAF
L - lumbricals (1st/2nd)
OAF = thenar muscles
O = opponens pollicis
A = ABductor pollicus brevis (adductor by ulnar nerve) , abductor longus via radial nerve
F = Flexor pollicis brevis (superficial head)

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4
Q

What muscles does the ulnar nerve innervate distal to the wrist?

A 
Adductor pollicius 
DEEP head of flexor pollicis brevis 
Dorsal / palmar interossei 
Medial two lumbricals 
Hypothenar muscles (abductor, opponens, flexor)
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5
Q

What is the cause of Klumpke’s palsy mechanically and what defect is typically seen?

A

Traction / forced abduction of arm -> i.e. catching a treebranch in adulthood or forcing arm upward during delivery of an infant

Total claw hand is seen: loss of medial and lateral lumbricals

  • > extension and MCP joints and flexion and PIP and DIP joints
  • > wrist is also extended (loss of FCU)

-> ulnar nerve and distal median nerve lost

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6
Q

What is thoracic outlet syndrome and what causes it?

A

Compression of lower trunk of the brachial plexus (like Klumpke’s palsy) also with involvement of subclavian vessels

Causes: Pancoast tumor, cervical rib (rib growing from C7)

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7
Q

What are the two types of supracondylar fractures, and which is most common? How do you tell them apart?

A

Extension - most common - line of humerus will be anterior to capitulum on X-ray

Flexion - line of humerus will be posterior to capitulum (end of humerus) on X-ray -> indicates arm was flexed during injury

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8
Q

What nerves are injured in extension type supracondylar fractures? What direction will injure each?

A

Extension type: Humerus is displaced anteriorly -> damage nerves anterior to elbow.

Anteromedial -> median nerve is injured
Anterolateral -> radial nerve is injured

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9
Q

What are the symptoms of the ulnar nerve intrapments?

A

Sensory deficits over medial 1.5 fingers, loss of interossei, and clawing of fingers 4/5 (FCU is preserved but lumbricals are not)

Positive Tinel’s sign at elbow for cubital tunnel syndrome, or wrist for Guyon canal.

Tinel = tapping

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10
Q

What is a Greenstick fracture and who gets it?

A

Common pediatric fracture
-> fracture extends partway through the width of the bone
-> half broken, half bent
(bent like a green twig)

A torus fracture is a buckle fracture of immature bone

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11
Q

What makes up the roof, floor, ulnar wall, and radial wall of the carpal tunnel?

A

Roof - transverse carpal ligament
Floor - proximal carpal row (scaphoid, lunate, triquetrum, pisiform)
Ulnar wall: pisiform and hook of hamate
Radial wall: scaphoid and trapezium

Ulnar and radial walls are the most lateral bones from each row

Remember it’s the proximal carpal row b/c lunate can drop into the carpal tunnel and cause carpal tunnel syndrome!

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12
Q

What typically causes a scaphoid fracture and how can you tell when it has happened?

A

Falling on outstretched hands

Anatomical snuffbox will be palpable

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13
Q

What is the origin, insertion, innervation and action of TFL?

A

Origin: ASIS
Insertion: Iliotibial tract
Innervation: Superior gluteal nerve (L4-S1)
Action: hip abduction

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14
Q

What does the femoral nerve supply motor to?

A

Iliopsoas - hip flexors
Pectineus - flexor and adductor of thigh
Quadriceps - leg extensors
Sartorius - Hip and knee flexor

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15
Q

What are the origin and action of the rectus femoris?

A

Origin: Anterior INFERIOR iliac spine (AIIS)
Action: Extension of leg and SOME FLEXION of the thigh (only quad muscle to cross the hip joint)

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16
Q

What is the origin, insertion, innervation, and action of the sartorius muscle?

A

Origin: ASIS (only other one other than TFL)
Insertion: pes anserinus (medial tibia)
Innervation: Femoral nerve
Action: Thigh flexion and leg flexion

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17
Q

What is the origin, insertion, innervation, and action of the pectineus muscle?

A

Origin: Superior pubic ramus
Insertion: Pectineal line - Proximal femur just inferior to lesser trochanter
Innervation: Femoral nerve
Action: Adduction of thigh, as well as weak flexor

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18
Q

What is the origin, insertion, innervation, and action of the biceps femoris?

A

Origin: Ischial tuberosity (like all hamstring muscles)
Insertion: Head of the FIBULA
(just remember that membranosus / tendinosus insert on the medial side, so femoris must insert laterally on the fibula)
Innervation: Long head by tibial division of sciatic nerve, short head by common peroneal division
Action: Long head extends thigh, both flex the leg

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19
Q

What provides sensation to the superior lateral back of leg and dorsum of the feet?

A

Superior lateral leg -> a branch of the common peroneal nerve.

Dorsum of the feet -> superficial peroneal (branch of the common peroneal nerve)

Between digits 1 and 2 -> deep peroneal nerve (branch of common peroneal)

Sural nerve (branch of tibial nerve) supplies inferior posterolateral leg and soles of feet.

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20
Q

What happens if the common peroneal nerve is injured?

A

Loss of tibialis anterior function, as well as loss of sensation on upper lateral leg and dorsum of the foot.

Think PED:
Peroneal Everts + Dorsiflexes
-> loss = FOOT DROP. Foot will be plantarflexed and inverted at rest.

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21
Q

What’s the McMurray test checking for and what does each way mean?

A

Medial / lateral meniscus tear

Pain / popping with lower leg in internal rotation -> lateral meniscus tear

Pain / popping with lower leg in external rotation -> medial meniscus tear

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22
Q

What are the two components of the sciatic nerve and what nerve roots does it come from?

A

Sciatic nerve comes from L4-S3

Common peroneal - L4-S2
Tibial - L4-S3

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23
Q

What is Sinding-Larsen-Johansson syndrome?

A

Adolescents who play jumping sports often get chronic pain at the INFERIOR POLE of the patella (requires hard extension of the leg when jumping)

Treat with rest and NSAIDs

Think “S-O” from patella-tibia
O = Osgood-Schlatter

or S = Superior

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24
Q

What is the cause of a high ankle sprain and what is disrupted?

A

External rotation injury

Disruption of the syndesmosis that holds the tibia and the fibula together distally (fibula makes lateral malleolus which btw runs further inferior than the medial malleolus)

Syndesmosis composed of two ligaments:

  1. Anterior inferior tibiofibular ligament (AITFL)
  2. Posterior inferior tibiofibular ligament (PITFL)
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25
Q

What are the two most common ligaments injured in low ankle sprain, and how are they injured?

A

ATFL - anterior talofibular ligament -> falling on plantarflexed and inverted foot

CFL - calcaneofibular fibular ligament -> falling on dorsiflexed and inverted foot

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26
Q

What test is used to differentiate between an ATFL and CFL low ankle sprain?

A

Anterior drawer test of the foot.

If you can pull the foot anteriorly when it’s in plantarflexion -> ATFL injury

If you can pull the foot anteriorly when it’s in dorsiflexion -> CFL injury

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27
Q

What does herniation of the disc between L4/L5 cause?

A

L5 pathology:
Deep peroneal nerve (primarily L5, to tibialis anterior) is affected

Weakness of dorsiflexion, difficulty in heel-walking

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28
Q

What does herniation of the disc between L5/S1 cause?

A

S1 pathology primarily:

Decreased achilles reflex (tibial nerve affected), weakness of plantar flexion, and difficulty of toe walking

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29
Q

What is ape hand?

A

Lack off abduction / opposability of thumb due to injury of recurrent median nerve
-> thumb can only be adducted (ulnar nerve)

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30
Q

Are the claw deficits more pronounced at proximal or distal injuries of ulnar / radial nerves?

A

Distal - since extrinsic flexors will make obvious the loss of lumbricals by pulling on the fingers
-> will be extension and MCP and flexion at DIP / PIP (opposite of normal)

-> these are called median / ulnar claw

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31
Q

What is Pope’s blessing vs OK gesture?

A

Pope’s blessing - proximal median nerve lesion -> hand gesture seen on making fist

OK gesture - proximal ulnar nerve lesion -> hand gesture seen on making fist

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32
Q

Where does disc dislocation usually occur?

A

Posterolaterally (weak / thin posterior longitudinal ligament)

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33
Q

What artery associates with the tibial nerve near the medial malleolus?

A

Posterior tibial artery

-> termination of popliteal artery

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34
Q

What type of enzymes carry out phase 1 drug metabolism? Phase 2?

A

Phase 1 - Cytochrome P450 mono-oxygenases

Reduction, oxidation, and hydrolysis

Phase 2 - Methylation, Sulfation, Glucuronidation, Acetylation

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35
Q

What toxin is found in reef fish like barracuda, snapper, and moray eel? What is its mechanism of action?

A

Ciguatoxin - opens Na+ channels, causing depolarization

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36
Q

What are the symptoms of ciguatoxin poisoning?

A

GI side effects
Perioral numbness
Reversal of hot/cold sensations
Bradycardia, heart block

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37
Q

What is the treatment of lead poisoning?

A

EDTA > dimercaprol (normally used for arsenic) > succimer

Use succimer in children -> It “Sucks” to be a kid who eats lead

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38
Q

What is a key side effect you should associate with griseofulvin, other than CYP induction?

A

Disulfiram-like reaction
-> not in sketchy, but think of the tin man with greasy alcohol being poured down his throat

Can also happen with “procarbazine”, a random antineoplastic

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39
Q

How is Babesia microti transmitted and how can it be differentiated from malaria symptomatically? What is the biggest risk factor for severe disease?

A

via the Ixodes tic (think of Robin of Ixodes amongst the vampires)
-> fever does not follow regular cycles

Risk factor = sickle cell disease (Severe hemolytic anemia). This is in contrast to malaria, where sickle cell disease is protective.

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40
Q

What are the treatments for Trypanosoma brucei infection?

A

Melarsoprol - mela “soap” - in sketchy, for CNS infections - “mela”tonin = sleep

Suramin - sounds like bottle of serum, for blood infection

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41
Q

What are the two forms of Leishmaniasis and where does the protozoa live inside the body?

A

Visceral (Donovan, black fever “kala-azar”) and Cutaneous (Braziliensis, brazil flag, zombie is flesh-eating)

Protozoa lives as amastigotes inside macrophages (goats in macrophage cages) -> characteristically multiple in macrophages

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42
Q

What are the symptoms of cutaneous and visceral leishmaniasis?

A

Cutaneous - skin ulcers

Visceral / Kala-Azar - Spiking fevers, pancytopenia (think of pan with RBCs in it), and hepatosplenomegaly (from macrophage involvement). Basically think of infected macrophages crowding out the bone marrow

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43
Q

What gram negative bug is pretty similar to Listeria and how is it spread? Is it encapsulated / what shape is it?

A

Yersinia enterocolitica (Think English terrier) -> is resistant to cold temperatures, and is thus able to multiply in stored blood transfusions

Like Listeria, spread via contaminated milk (think of the Toddler holding the bottle of milk), or via pet feces (especially puppies)

It is an encapsulated gram negative organism that exhibits bipolar (safety pin) staining

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44
Q

What disease does Rickettsia prowazekii cause and how does the rash spread?

A

Causes epidemic typhus - spread by lice

Just remember Typhus on the Trunk, or how the football coach directs his players from the center outward.

Another major difference from Rickettsia ricketsii is that it spares the palms and soles (football players with white hands)

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45
Q

What is the vector for Trypanosoma brucei and what are the two subspecies? What disease does it cause? Which is worse?

A

Causes African sleeping sickness - Tsetse fly vector (think of the tea next to the sleeping girl)

  1. West African - gambiense - Gambia. Way more indolent, human reservoir only.
  2. East African - rhodesiense - Rhodesia is an old name for Zimbabwe. Way more fulminant, and reservoir is animals.
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46
Q

What are the symptoms of T. brucei?

A

Alot like brucellosis, oddly enough!
Undulating / recurrent fever -> due to constant antigen variation
Coma
Enlarged cervical (Winterbottom’s sign) / axillary lymph nodes (necklace and sleeves of girl)

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47
Q

How is Chagas disease treated?

A

Nifurtimox - Knee high fur moccasins
or
Benznidazole

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48
Q

What are the side effects of primaquine?

A

Hemolysis in G6PD

There is no sketchy symbol for this, it’s just fact in First Aid and was mentioned in sketchy

Remember primaquine (primal queen) is the drug added to treat the hypnozoites of VivAX and OVALe

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49
Q

What is the form of malaria which is best visualized in Giemsa stain?

A

Ring form = immature schizont (Trophozoite ring).

Remember. Merozoite infects RBC -> trophozoite -> immature schizont -> Schizont -> merozoite release

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50
Q

Which species cause hepatic / intestinal schistosomiasis vs urinary schistosomiasis? How do their eggs look?

A

Hepatic / intestinal - S. mansoni (lateral spine next to man) and S. japonicum (circular / spineless, like japanese flag circle - Japanese sun is smooth)

Urinary - S. haematobium (long terminal spine, like a swordfish)

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51
Q

What virus is likely to cause jaundice, back pain, and bloody diarrhea?

A

Yellow fever, a type of Flavivirus
-> think of the ox with the live attenuated vaccine coming out of his back

Flavi = Yellow = Jaundice

Also has black vomitus associated with it, and councilman bodies in liver (causes jaundice)

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52
Q

What are the components of Env? Their function?

A

Think ENVoy:

Gp160 - cleaved by protease into gp120 and gp41

Gp41 is a transmembrane protein to help with FUSION
-> gp41 grappling hooks, blocked by enfuvirtide

Gp120 is a docking protein which interacts with CD4 as well as CCR5 (macrophages, T cells) or CXCR4 (T cells) depending on early / late infection, respectively. Think of the GP120 battering ram!!

Explains why homozygous CCR5 mutations will be immune to HIV infection.

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53
Q

What are the components of Gag and their function?

A

Capsid (p24) -> surrounds the 2 RNA strands. Think of the wizard hat with two RNA dragons inside it, with the brim like a sundial -> 24 hours in a day.

Matrix (p17)

Also p7 - nucleocapsid protein. Think 24 hours a day, 7 days a week

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54
Q

What are the components of Pol and their function?

A
  1. Protease - maturation
  2. Integrase - integration into genome
  3. Reverse transcriptase - synthesis of dsDNA for integration
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55
Q

How should HIV be diagnosed in neonates?

A

Use PCR amplification tests. ELISA / Western blot would definitely come back positive since HIV positive mothers passively transfer their IgG antibodies across the placenta and it takes a while for these numbers to decrease

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56
Q

How does Hantavirus do damage?

A

Pulmonary capillary leak -> think of Paul Bunyan’s sweaty shirt
Leads to pre-renal azotemia

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57
Q

What are the unique characteristics of Arenavirus and what is its most famous subtype?

A

Ambisense (ambidextrous) - both positive and negative RNA virus
-> circular with two segments (two gladiators fighting in circles)
Rodents are the reservoir

Causes LCV -> lymphocytic choriomeningitis virus (aseptic meningoencephalitis)

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58
Q

What is the structure of polyomaviruses? Is it enveloped?

A

Circular dsDNA virus which has NO envelope (JC’s robe is falling off)

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59
Q

What is the process of replication for Hepatitis B virus?

A

Partially dsDNA genome enters the cell and promptly enters the nucleus.

Upon entering the nucleus, P protein finishes transcription to a dsDNA circular genome.

Host (human) DNA-dependent RNA polymerase makes a + sense RNA from the viral - sense DNA.

+ sense RNA is used to make viral proteins in the cytoplasm, as well as P-protein acts upon it via reverse transcriptase to synthesize - sense DNA. It also acts in a DNA-dependent method to make it partially double-stranded, and replication is complete.

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60
Q

What are the features of Donovanosis (Klebsiella granulomatis) and how is it told apart from LGV?

A

Starts as a painless, beefy red ulcer.
Donovan bodies will be present in the cytoplasm (K. granulomatis) similar to the intracytoplasmic bodies of LGV.

However, Donovanosis is NOT associated with painful lymphadenopathy, unlike LGV

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61
Q

What chromosome is associated with ADPKD2?

A

4 - same as Huntington

16 is ADPKD1 and alpha-thalassemia

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62
Q

How do you tell Edwards syndrome and Down syndrome apart via Quad screen?

A

Down syndrome: decreased aFP, INCREASED B-hCG, decreased estriol, INCREASED inhibin A

Edwards syndrome: decreased aFP, DECREASED B-hCG, decreased estriol, DECREASED or NORMAL inhibin A

Down syndrome is only one where Beta-HCG will be increased

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63
Q

What chromosome is associated with Wilms tumor?

A

11

Remember, Beckwith-Wiedmann is 11p15 and is associated

Beckw1th-W1edmann

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64
Q

What chromosome is associated with Rb1 and BRCA2?

A

13 - same as Wilson / Patau

Remember that BRCA1 and p53 are associated on the same chromosome as NF-1

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65
Q

What is Chlorpropamide vs Chlorthalidone vs Chlorpromazine vs Thioridazine?

A

Chlorpropamide - 1st generation sulfonylurea, with tolbutamide

Chlorthalidone - Long acting thiazide diuretic

Chlorpromazine - Low potency 1st generation antipsychotic associated with Corneal deposits

Thioridazine - Low potency 1st generation antipsychotic associated with reTinal deposits

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66
Q

What receptor type do FSH, LH, ACTH, TSH, CRH, and hCG use?

A

Gs -> cAMP

All of anterior pituitary except GH and PRL -> mammosomatotrophs signal through JAK-STAT pathway

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67
Q

What receptor type do GnRH, Oxytocin, and Gastrin use?

A

Gq -> remember it signals thru IP3 just like the M3 receptor

-> oxytocin is posterior pituitary like ADH, which signals thru V1 receptor to vasculature, which is Gq

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68
Q

What does a VIPoma do and why?

A

Watery diarrhea, hypokalemia, achlorhydria

  • > “pancreatic cholera”
  • > in addition to being necessary for LES relaxation, it also DECREASES gastric acid secretion, and greatly increases electrolyte secretion by pancreatic ducts (“VASOACTIVE”).
  • > improves intestinal motility with secretions
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69
Q

Is hemoglobin positively / negatively charged which affects its migration?

A

Negatively! Thus migrates towards the positively charged anode.
-> just remember anode attracts the negatives

Explains why things which increase positive charge (i.e. glutamate -> lysine) in hemoglobin C -> decrease migrations.

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70
Q

What is the calculation for oxygen content of blood?

A

mL O2 / dL blood = (1.34 * Hb * SaO2) + (0.003 x PaO2)

1st half of equation is oxygen bound to Hb:

Hb = 15 g/dL average
1.34 mL O2/gram Hb
SaO2 is the hemoglobin saturation %

2nd half of the equation is the oxygen dissolved in plasma alone:

0.003 mL O2 / mmHg O2.

Normal ~20 mL O2/ dL blood. Multiply by CO to get oxygen delivery

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71
Q

What is the alveolar gas equation?

A

PAO2 = PIO2 - PaCO2 / R

R = VCO2 / VO2 -> usually 0.8

PIO2 = (760-47)*0.21 = 150 mmHg usually

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72
Q

What are average ICF / ECF volumes relative to body weight?

A

60-40-20 rule

60% = total body water 
40% = ICF 
20% = ECF
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73
Q

What is the approximate Tm for glucose? What is Tm?

A

Tm = 375 mg/min, average ability of a tubule to reabsorb glucose (attempting to compensate for GFR * plasma concentration, aka the filtered load)
-> remember that Tm is the sum of all transporters abilities in a tubule

Threshold is where first tubules start to fail = 200 mg/dL, then by 300 mg/dL splay has finished and the tubules are 100% saturated.

300 mg/dL * 125 mL / min * (1/100 dL/mL) = 375 mg/min filtered load.

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74
Q

What electrolyte disturbances can hypomagnesemia cause and how?

A

Hypokalemia - Mg+2 needed to inhibit ROMK
-> hypokalemia also causes nephrogenic DI, TdP arrhythmia

Hypocalcemia - Mg+2 needed to inhibit CaSR -> tetany
-> also prolongs the QT (Ca+2 needed to inactivate L-type calcium channel)

-> HypERcalcemia causes nephrogenic DI

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75
Q

What is dilutional hyperchloremic acidosis? Where does this appear in the mnemonic for normal anion gap metabolic acidosis?

A

Rapid ECF expansion via NaCl will dilute out the current concentration of HCO3-, making the body relatively acidic

HARDASS 
Hyperalimentation - high H+ + Cl- levels in food 
Addison disease - Type IV RTA 
Renal tubular acidosis 
Diarrhea - HCO3- / K+ loss 
Acetazolamide - Type II RTA 
Spironolactone - Type IV RTA 
Saline infusion - Dilutional
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76
Q

What are the periods of lung development up until age 20? What develops in each of these stages?

A

Lung bud = 4-6 weeks - up to segmental bronchi
Pseudoglandular period = 6-16 weeks - up to terminal bronchioles
Canalicular period = 16-26 weeks - up to alveolar ducts
Saccular / Alveolar period = 26 weeks to term - up to terminal sacs
Alveolar period = birth to 10 years - up to adult alveoli number

10-20 years - HYPERTROPHY of existing alveoli

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77
Q

How is PDH deficiency inherited and what are its clinical symptoms? How is it treated?

A

X-linked
Neurologic defects, with lactic acidosis and increased serum alanine starting in infancy
Treatment: Ketogenic diet, with increased lysine and leucine (purely ketogenic)

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78
Q

Tell me how the following agents inhibit the ETC:

  1. Rotenone
  2. Antimycin A
  3. Oligomycin
  4. Aspirin overdose
A
  1. RotenONE - inhibition of complex 1
  2. Antimycin A - inhibition of complex 3. “Ant-3-mycin”
  3. Oligomycin - remember the Fo subunit of ATP synthase -> inhibits ATP synthase (o=oligomycin sensitivity)
  4. Aspirin overdose - uncoupling agent, like 2,4-DNP
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79
Q

What are the symptoms of lower lateral pontine syndrome?

A

“Facial droop, AICA’s pooped”

facial paralysis, dry eye (facial nerve is PANS to lacrimal gland), decreased salivation (loss of sublingual / submandibular), loss of taste on anterior 2/3, deafness (CN8), nystagmus to opposite side (no input from ipsilateral side, fast reset the other way)

Signs similar to PICA - Horner syndrome may also occur, as well as loss of contralateral ALS and ipsilateral spinal nucleus of V

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80
Q

Where do vessels proliferate in wet ARMD?

A

choroid layer -> responsible for supplying blood to outer 1/3 of retina
-> neovascularization can be stopped via ranibizumab or bevacizumab

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81
Q

What causes inferior alternating hemiplegia (mid medullary syndrome)? Symptoms?

A

Infarct of proximal branches of anterior spinal artery as it comes off of vertebral artery, or vertebral artery branches

-> loss of blood supply to mid medulla level -> 10-12 M and M’s, remember

Inferior alternating hemiplegia = contralateral UMN signs + CN12 palsy (ipsilateral tongue deviation) -> also called medial medullary syndrome

Loss of medial lemniscus -> decreased contralateral proprioception as well (internal arcuate fibers already crossed)

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82
Q

How do nafcillin and ampicillin differ with regards to resistance?

A

Ampicillin - still penicillinase sensitive, just wider spectrum. Needs to be combined with a Beta-lactamase inhibitor to retain activity

Nafcillin - Penicillinase resistant, narrower spectrum. Works by having a bulky R group which is not cleaved by penicillinases, but MRSA is still resistant due to altered penicillin-binding protein

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83
Q

What is the usage of the 5th generation cephalosporin and what is it called? Does it have Pseudomonas coverage?

A

Think of General Tara knocking over the emperor -> only cephalosporin to have MRSA coverage

NO Pseudomonas coverage -> not next to the poster.

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84
Q

What are the mechanisms of resistance to cephalosporins?

A
  1. Altered PBPs

2. Extended spectrum beta lactamases - (they are generally resistant to normal beta lactamases due to side changes)

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85
Q

How are tetracyclines eliminated, and why are expired ones an issue?

A

Eliminated fecally, so safe to use in renal failure -> think of the colonic poop tube in the back.

Expired ones are hella problematic cuz they can cause Fanconi syndrome (proximal absorption defect, including a Type II RTA).

86
Q

What is a common treatment regimen for severe polymicrobial infections of the female genital tract (i.e. endometritis)?

A

Clindamycin + gentamicin -> think of the karate lady doing Pec fly’s with the ovaries while having psi’s in her pockets

87
Q

What drugs are used for the treatment of Mycobacterium avium complex?

A
  1. Macrolide - Clarithromycin or azithromycin
  2. Ethambutol - Think Ethyl the Sheriff with her AIDS ribbon
  3. Rifabutin - think “Buttes” - mesas, a drug related to rifampin but less problematic for CYP induction in patients already being treated for HIV
88
Q

Which fluoroquinolones are useful for treating pseudomonas and when are these drugs indicated for the treatment of UTIs? Pyelo?

A

Think of Mona Lisa elevating and sipping her UTI cup -> Levofloxacin and Ciprofloxacin, but NOT moxifloxacin

Cipro / Levo good for complicated UTIs or prostatitis. First line is TMP / SMX.

Think of the kidney canteen spilling out -> FQs are 1st line in the empiric treatment of pyelonephritis

89
Q

What are the consequences of renal toxicity of amphotericin B?

A
  1. Type 1 renal tubular acidosis - Distal RTA with hypokalemia -> Think of 1 acidic test tube, slipping on banana peel
  2. Hypomagnesemia - should supplement. Remember that very low magnesium and can lead to low PTH -> hypocalcemia
  3. Anemia -> broken kidney leads to decreased erythropoieitin synthesis
  4. Prerenal azotemia - from pores formed in kidney and volume loss. Always give with saline.
90
Q

What is the unique side effect of emtricitabine? What drug class is it?

A

Hyperpigmentation of palms and soles -> think of Arthur’s “excalibur” and the gloves he’s wearing

Drug class - NTRI

Note: Delavirdine is an NNRTI which sounds like an NRTI

91
Q

What are the two main side effects of ribavirin to remember? One of these “side effects” is broadly similar to a concern of griseofulvin.

A
  1. Dose-dependent hemolytic anemia - think of the rupturing tomatoes
  2. Teratogenic!!!! - just like griseofulvin (which is also a CYP inducer and causes a disulfiram reaction)
92
Q

What is the first step in activation of acyclovir and why is this important?

A

The guanosine (think gucci bag) analog is phosphorylated by Hermes (VIRALLY encoded thymidine kinase)

  • > important because initial phosphorylation step only occurs in virally infected cells, which allows for interference.
  • > only HSV/VZV has the thymidine kinase, it is not present in CMV / EBV -> acyclovir ineffective in these cells
93
Q

What is the mechanism of action of Cidofovir? What drug is similar?

A

NucleoTide analog which does not require viral activation

-> along with Foscarnet, can directly target polymerases with kinase activation of any kind

Think of Cid dragging his car in to turn off the polymerase

94
Q

When is foscarnet used and what are its big side effects?

A

Only for CMV when ganciclovir is not available

Side effects: Nephrotoxicity (think of barrel of kidney beans falling over), CNS effects -> boy seizing, potential chelator of divalent cations in blood -> hypocalcemia, hypokalemia, hypomagnesemia

95
Q

What is the mechanism of foscarnet-induced electrolyte disturbance? Include how hypomagnesiemia causes hypokalemia?

A

Pyrophosphate analog -> binds free calcium -> hypocalcemia

Hypomagnesemia -> decreased GI absorption

Magnesium is required to decrease the activity of ROMK in the kidneys. Hypomagnesemia -> hypokalemia.

96
Q

What causes Familial Mediterranean fever? What is the hallmark of the condition

A

Autosomal recessive mutation in pyrin, a regulator of pro-inflammatory cytokines. Leads to recurring fever, joint pains, and serositis with overproduction of IL-1 -> systemic accumulation of AA amyloid (SAA)
-> this is a neutrophil dysfunction disorder

97
Q

What mediates adhesion? What upregulates this?

A

Firm attachment, high affinity interaction between VCAM-1 and ICAM-1 (integrin ligands) of endothelial cells and ligands on leukocytes.

ICAM/VCAM are upregulated via IL-1 and TNF.
Ligands = Integrins. Upregulated by LTB4 and C5a, they neutrophil chemoattractant agents

ICAM = intercellular adhesion molecule

98
Q

What is the triad of AIRE loss / autoimmune polyendocrine syndrome?

A

APS-1:

  1. Autoimmune adrenalitis - Addison’s
  2. Autoimmune parathyroiditis - hypoparathyroidism
  3. Recurrent candida infections - Chronic mucocutaneous candidiasis
99
Q

What are the typical causes of death in late-stage lupus?

A

Renal failure, infection (due to immunosuppressive therapy), or accelerated coronary artery atherosclerosis
-> alot like diabetes in the fact that atherosclerosis is scary

100
Q

What three cancers is ionizing radiation a risk factor for? Mechanism?

A

AML, CML, and papillary carcinoma of the thyroid

-> generation of hydroxyl free radicals which breaks double-stranded DNA

101
Q

What are the three C’s of Wecener’s (Wegener / Granulomatosis with polyangiitis)?

A

C distribution - nasopharynx, lungs, kidneys
C-anca
Cyclophosphamide / corticosteroids is the treatment
-> same as polyarteritis nodosa

102
Q

Where does aortic dissection typically occur and why is HTN the most important cause?

A

Occurs in the first 10 cm of the aorta which is under high stress. You need weakening of the tunica media for this to occur.

Media is particularly thick in the first 10 cm. In HTN, hyaline arteriolosclerosis of the vasa vasorum occurs -> poor blood supply to the media -> atrophy and weakness of the media

103
Q

What congenital heart defect is particularly associated with fetal alcohol syndrome?

A

Ventricular septal defect -> the most common congenital heart defect

104
Q

What type of coarctation of the aorta is associated with Turner syndrome? What happens in conjunction with it? Physical exam finding on presentation?

A

Infantile or pre-ductal coarctation (stenosis proximal to the ductus arteriosus)

This occurs in conjunction with PDA, because pressure in aorta will not be high enough to close the PDA.

Presents with upper extremity hypertension (aortic arch) and lower extremity cyanosis (due to aortic pressure being so low where the ductus arteriosus is that blood can move from pulmonary to systemic circulation).

105
Q

Where does adult coarctation of the aorta occur and what anomaly is particularly associated?

A

Occurs post-ductal -> not discovered until adulthood because it is not assocatied with PDA / cyanosis.

Associated with bicuspid aortic valve (oddly enough, also seen in Turner syndrome)

106
Q

What is the cause of most dilated cardiomyopathy? What is the second most common cause?

A
  1. Idiopathic - cause unknown
  2. Genetic abnormalities (1/3 of cases) - autosomal dominant, usually affecting structural proteins of the myocardial cytoskeleton

You’re reading that right mate!

107
Q

What is the usual cause of hypertrophic cardiomyopathy?

A

USUALLY autosomal dominant mutations in sarcomere proteins leading to decreased cardiac myocyte contractility
-> growth-factor induced hypertrophy and fibrosis

So just to recap, dilated = cytoskeleton, hypertrophic = sarcomere

108
Q

What is Loeffler syndrome?

A

Endomyocardial fibrosis (infiltration of endocardium + myocardium) with an eosinophilic infiltrate and peripheral eosinophilia.

It is a cause of restrictive cardiomyopathy.

-> usually occurs secondary to cardiac damage by eosinophils fighting a parasitic (i.e. Ascaris) infection, with release of major basic protein which is toxic to heart.

109
Q

How do non-DHP/DHP’s cause negative cardiac inotropy and smooth muscle relaxation, respectively, but no effect on the skeletal muscle?

A

L-type calcium channel is the primary channel on smooth muscle which controls Ca+2 influx to activate the calcium-calmodulin complex

Skeletal muscle does not rely on Ca+2 current as its primary source of contraction -> blockade of L-type calcium channel does not interrupt Ca+2 channel and RyR connectivity

110
Q

What is the mechanism of action of fish oil in improving cardiovascular outcomes?

A

It’s included in the niacin / fibrate sketch, so you know it has to lower VLDL

The omega-3-fatty acids suppress hepatic VLDL reduction and may reduce cardiovascular risk.

111
Q

A patient comes in with a locally aggressive and destructive benign neoplasm of the nasopharynx causing epistaxis. Name and describe his condition, and what demographics he most likely is?

A

Nasopharyngeal angiofibroma (it is aggressive despite being benign)

Highly vascular neoplasm which causes profuse bleeding and has a high recurrence rate

Almost exclusively in adolescent males, especially with fair skin and red hair

NOSE-BLEEDING GINGER

112
Q

What is the usual cause of laryngeal vs pharyngeal/oropharynx squamous cell carcinoma?

A

Laryngeal - usually due to alcohol / tobacco

Oropharynx - usually due to HPV 16
-> includes tonsils, soft palate, base of tongue, pharynx

113
Q

Are hypoxemia and cor pulmonale more common in emphysema or chronic bronchitis?

A

More common in chronic bronchitis, where air trapping behind mucus plugs is more likely to lead to hypercapnia -> hypoxia -> vasoconstriction. This leads to early cor pulmonale.

Hypoxemia is a LATE complication of emphysema due to elastase destroying blood vessels in the interstitium -> reduction in gas exchange -> pulmonary hypertension and subsequent cor pulmonale.

114
Q

What is the cause of airway obstruction in bronchiectasis?

A

Dilation of the airways -> airflow becomes more easily turbulent in the large airways -> air just begins to swirl around in the open tube when attempted to exhale and never leaves

-> associated with aspergillosis in asthmatics and CF patients

115
Q

What are two characteristic pathologic findings of Sarcoidosis which are not non-caseating granulomas?

A
  1. Asteroid bodies - look like little spokes in a stellate shape - a funny configuration of giant cells
  2. Schaumann bodies - calcium and protein inclusions as part of a giant cell reaction -> basically look like DCIS or Psammoma bodies within a noncaseating granuloma
116
Q

What is the function of BMPR2?

A

Gene which normally inhibits vascular smooth muscle proliferation
-> inactivating mutation causes heritable pulmonary arterial hypertension

117
Q

What type of adenocarcinoma has a pneumonia-like presentation? Where does it grow?

A

BronchiOLOalveolar subtype of adenocarcinoma in
situ:
Grows along alveolar septae with apparent thickening of alveolar walls. Tall, columnar cells containing mucus

Pneumonia-like presentation because CXR shows hazy infiltrates and patients often present with bronchorrhea (copious amounts of watery sputum from mucus production)

118
Q

Are bronchioloalveolar carcinoma, large cell carcinoma, small cell carcinoma, and carcinoid tumor related to smoking?

A

Bronchioloalveolar subtype of AIS - NOT related to smoking

Carcinoid tumor - NOT related to smoking

Small cell carcinoma - starts with S - YES related to smoking

Large cell carcinoma - the exception - YES! related to smoking

119
Q

Are metastases to the lung common? Which two cancers most frequently metastasize there?

A

More common than primary tumors

  1. Breast
  2. Colon
120
Q

What are two situations in which DLCO may actually be increased?

A
  1. Increased hemoglobin in alveoli - i.e. Goodpasture syndrome -> alveolar hemorrhage
  2. Increased pulmonary capillary blood volumes
    - > i.e. congestive heart failure, polycythemia, etc
121
Q

Give two useful tumor markers for mesothelioma?

A
  1. Cytokeratin - also called tonofilaments
  2. Calretinin - in the Troponin C family

Taken together, can differentiate mesotheliomas from other peripheral / pleural lung cancers or things which would spread to the region

-> will also be associated with long, slender microvilli

122
Q

What are dinoprostone and carboprost analogs of and used for?

A

Think of the guy with the dino hat in the extreme sports section - PGE analog. He is holding a uterus bag.
-> Dinoprost used for ripening of the uterus / stimulation of uterine contraction

Carboprost - think of cardboard box kid in the “F”ootwear section. PGF2alpha analog
-> Used for uterine contraction but also control of uterine bleeding by clamping down on blood vessels

123
Q

What is the main advantage of the CysLT1 receptor blockers and what types of asthma are they especially good for?

A

Zafirlukast / Montelukast block the most potent leukotriene bronchoconstrictor -> LTD4

They are orally taken agents - good for those poorly compliant with inhaled therapy
Good for:
1. Aspirin-induced - arachidonic acid diverted to leukotriene pathway
2. Exercise-induced asthma - just remember the lacrosse player

124
Q

What is the treatment for ITP?

A

Treatment - corticosteroids, IVIG (short-lived distraction for macrophages), or splenic removal if refractory

Splenic removal -> removes the SOURCE of the antibodies and the SITE of removal

125
Q

What drug is given in the management of HIT?

A

Direct thrombin inhibitors, i.e. espectially argatroban (gator eating thrombeaver)

126
Q

What condition does overactivity of plasmin cause? Give two example causes of this.

A

Disorders of fibrinolysis - plasmin overactivity. Leads to excessive cleavage of serum fibrinogen.

  1. Radical prostatectomy - release of urokinase activates plasmin
  2. Cirrhosis of liver - reduced production of alpha2-antiplasmin
127
Q

How do you differentiate disorders of fibrinolysis from DIC based on labs?

A

PT/PTT will still be elevated - plasmin destroys coag factors
Bleeding time will be elevated - inhibits platelet aggregation
Platelet count will be NORMAL - clots not forming
Fibrinogen split products are increased WITHOUT D-dimers -> plasmin is cleaving fibrinogen without the full maturation of the clotting cascade

128
Q

How do thrombomodulin and tissue factor pathway inhibitor (TFPI) work?

A

Thrombomodulin -> binds thrombin, activates protein C and protein S -> degrades factors 5 and 8 which are needed for coagulation pathway

TFPI - inhibits interaction between TF-7a complex and X

-> secreted by healthy endothelium as normal defenses, along with tPA and heparin-like molecules

129
Q

What is the second most common inherited hypercoagulability disorder in Caucasians and what causes it?

A

Prothrombin gene mutation

  • > point mutation in 3’-UTR what causes overexpression of prothombin
  • > increased prothrombin levels leads to hypercoagulability
130
Q

What is the femoral sheath and what structures are contained within it?

A

Sheath made by transversalis fascia which surrounds the artery, vein, and lymphatics of the structures in the femoral triangle, but NOT the nerve

131
Q

What is the difference between an erosion and an ulcer?

A

Erosion - loss of mucosa of the stomach, not into the submucosa (last layer of mucosa is muscularis mucosa)

Ulcer - Penetration into the sUbmucosa or deeper

132
Q

What are the pleuropericardial folds?

A

Two lateral folds forming ventrally from the wall of the pericardioperitoneal canals, which grow medially and hold the right or left phrenic nerve + cardinal veins.

They will fuse with eachother and separate the pericardial cavity from the pleural cavity.

Basically, these are the folds which separate the heart from the pleural cavity.

133
Q

Where does the body of the uterus and cervix drain?

A

External iliac nodes, with the superior bladder (since these are structures located very high)

Inferior bladder / prostate / proximal vagina are all inferior so will drain to internal iliac

134
Q

What lubricant glands open immediately next to the urethra in females and what are they analogous to in the male?

A

Paraurethral glands of Skene

Analogous to prostate gland

135
Q

What derives the vestibular bulbs vs greater vestibular glands in females?

A

Vestibular bulbs - genital tubercle (analogous to corpus spongiosum in males)

Greater vestibular glands (Bartholin glands) - derived from urogenital sinus (analogous to bulbourethral / Cowper glands in males)

136
Q

What is the cause of an anterior urethral injury and where will the fluid leak?

A

Perineal straddle injury

Fluid leaks between Galludet’s (deep perineal) and Colle’s (superficial perineal) fascia, which is the “superficial perineal space”

Remember than Galludet’s is one layer superficial to the deep fascia of Buck which invests the ischiocavernosus / bulbospongiosus muscles.

137
Q

What populates the mucosa of the trachea and how is it different than a bronchus?

A
  1. Tall, pseudostratified columnar epithelium with goblet cells
  2. Lamina propria connective tissue with blood vessels (to warm the air)

Difference from bronchus - no muscularis mucosae, since the cartilage is so strong in the trachea, but discontinuous in the bronchi. Also, the epithelium transitions to simple ciliated columnar in the bronchi.

138
Q

What is spermiogenesis vs spermatogenesis?

A

Spermatogenesis - name for entire process overall. Starts with diploid spermatogonia (germ cells) dividing, which will become primary spermatocytes, and undergo meiosis to become spermatids (haploid).

Spermiogenesis - process of making haploid spermatids into haploid spermatozoa (mature sperm), gaining a tail, losing cytoplasm, and gaining acrosome

139
Q

What is arch 1&2 syndrome also called? What are its features and what causes it?

A

Treacher Collins syndrome - small lower jaw, facial defects, malformed ears. It is due to insufficient NEURAL CREST cells to Arch 1 and Arch 2

140
Q

What are the more specific toxicities of tacrolimus?

A
  1. Increased risk of diabetes + neurotoxicity as compared to cyclosporin
  2. NO gingival hyperplasia or hirsutism (vs cyclosporine)

Rest of side effects are the same (hyperlipidemia, nephrotoxicity)

141
Q

What is the non-calcineurin-inhibiting immunophilin and how does it work?

A

Sirolimus (rapamycin) - binds FKBP12 (similar to tacrolimus) but rather inhibits mTOR (mammalian target of rapamycin), a protein responsible for downstream signalling of IL-2. This will keep the cell arrested at G1 phase.

142
Q

What is Oprelvekin and what is it used for?

A

IL-11, used for treatment of thrombocytopenia (stimulates megakaryocytes)

Also used with Romiplostim and Eltrombopag

143
Q

What’s the mechanism of sirolimus derivatives (but not tacrolimus) in drug-eluting coronary stents?

A

Block the mTOR pathway -> prevent smooth muscle cell proliferation, “neointimal hyperplasia” which results in restenosis

144
Q

What is serum iron vs serum ferritin measuring?

A

Serum iron - amount of iron which is bound to transferrin within the blood

Serum ferritin - amount of iron stored in liver / bone marrow macrophages

145
Q

Give the two ways in which hepcidin causes anemia of chronic disease?

A
  1. Increases the degradation of ferroportin
  2. Decreases release of stored ferritin from bone marrow macrophages to erythroid precursors
    - > ferritin stores will be up.
146
Q

What does four alpha genes deleted cause in alpha thalassemia? What abnormal hemoglobins are present?

A

Hydrops fetalis

In utero: Hemoglobin Barts (gamma 4) seen on electrophoresis
Later in life: HgH (beta 4), if they survive

147
Q

What are the features of beta thalassemia anemia? What is seen on electrophoresis in minor / major?

A

Hypochromic, microcytic anemia with target cell formation

Minor: decreased HbA and mildly increased HbA2 (>4%) / HbF (>2%). >3.5% A2 is diagnostic.

Major: little to no HbA (20%), almost all HbA2 (4+%) / HbF (70+%)

148
Q

What happens if beta thalassemia is left chronically untreated?

A

Splenomegaly due to work hypertrophy

Excessive erythropoietin -> increased iron absorption and extramedullary hematopoiesis

Extramedullary hematopoiesis -> hepatosplenomegaly, “crew cut” skull changes and facial bone changes “chipmunk facies”

Anemia -> High output cardiac failure, growth failure

149
Q

What is the normal reticulocyte % and how do you correct it for anemia (i.e. the problem that loss of RBCs will artificially increase the reticulocyte % without a true increase in production)

A

Normal: 1-2%

Correct via multiplying reticulocyte % * hematocrit / 45

45 represents a normal hematocrit, so just normalizing the hematocrit for normal red cell mass.

> 3% corrected = adequate response, peripheral destruction
<3% corrected = underproduction

150
Q

How does the presentation of intravascular vs extravascular hemolysis differ clinically?

A

Both can present with increased urobilinogen / urobilin due to increased bilirubin production

Intravascular - presents with decreased haptoglobin (binding hemoglobin), schistocytes, and hemoglobinuria / hemosiderinuria

Extravascular - presents with NO hemoglobinuria / hemosiderinuria since uptake is by RES system. Splenomegaly due to hypertrophy.

151
Q

What happens to the RDW in hereditary spherocytosis and what causes hemolysis?

A

Blebbing of membrane leads to constant shrinking overtime (loss of structural proteins)

  • > older RBCs will be smaller
  • > high RDW due to age disparities

Hemolysis is extravascular by splenic removal because spherocytes cannot fit thru splenic sinusoids as they lose their disc shape

152
Q

What will happen in the skeleton in order to keep RBC production up in sickle cell anemia?

A

Massive erythroid hyperplasia -> same as thalassemia

-> crew cut appearance on Xray, chipmunk facies, hepatomegaly.

153
Q

What is the pathogenesis of acute chest syndrome?

A

Pulmonary vasculature vaso-occlusion, usually due to infection i.e. pneumonia

  • > pneumonia causes hyperemia and slowed transit time thru vessels -> hypoxemia -> increased sickling
  • > presents with chest pain, shortness of breath, and lung infiltrates
154
Q

What are two common causes of IgM-mediated AIHA and where does hemolysis occur?

A

IgM agglutinates RBCs in relatively cold temps of extremities -> fixes complement (IgM good at fixing complement) -> INTRAVASCULAR hemolysis

  1. Mycoplasmia pneumonia
  2. Mononucleosis (infectious)

-> IgG “warm” is generally EXTRAvascular hemolysis (generally drugs, lupus, or CLL)

155
Q

How is PCT treated?

A

Avoid ETOH consumption (hepatic toxin), avoid sun exposure (werewolf), phlebotomy to reduce iron levels
-> both porphyrias are treated with alcohol avoidance

156
Q

What is the most common cause of death in CLL? What does this do to blood counts as well?

A

Infections due to hypogammaglobulinemia - neoplastic B cells do not want to produce useful antibody

If they do, often causes autoimmune hemolytic anemia (leads to thrombocytopenia (Evan’s syndrome) and anemia) -> usually a Warm (IgG), but rarely Cold (IgM)

157
Q

What will physical exam and CBC show with HCL? Why do these things happen? Will there be lymphadenopathy?

A

Massive splenomegaly due to accumulation of hairy cells in red pulp

NO lymphadenopathy -> cells are TRAPPED in the bone marrow and cannot make it to LN’s

Pancytopenia will be the rule
-> due to massive fibrosis of bone marrow

158
Q

What are classical symptoms of essential thrombocythemia? Will it cause gout?

A

Usually asymptomatic, but may present with bleeding and thrombosis events, headache, lightheadedness, syncope

Classically does not cause hyperuricemia / gout like P. vera or CML -> not that much nuclear material in megakaryotes, just membrane blebbing which makes platelets.

159
Q

What does the peripheral blood smear show for PMF? Why?

A

Leukoerythroblastic smear - spleen is not built to hold all this hematopoesis so immature cells leak out, includes immature LEUKOBLASTS and ERYTHROBLASTS

Includes nucleated RBCs, and immature neutrophils

160
Q

What is the cause of hyperplasia of sinus histiocytes?

A

Lymph node draining a region of cancer
-> medullary region hyperplasia

Can also be seen idiopathic in Sinus histiocytosis with massive lymphadenopathy (Rosai-Dorfman disease)

161
Q

What types of antibody are responsible for the M spike in multiple myeloma? Most common cause of death in this disease?

A

IgG - 60% of cases
IgA - 20-25% of cases

Death - infection, due to lack of diversity in Ig’s
-> IgM would be Waldenstrom only

162
Q

What is MGUS? Why is it relevant?

A

Monoclonal gammopathy of undetermined significance
-> M spike - monoclonal spike on SPEP, but plasma cells are <10% in bone marrow and no CRAB symptoms. >10% would be smoldering myeloma.

  • MGUS is common in older patients, and progresses to multiple myeloma at a rate of 1% per year (precursor to MM)
163
Q

What drugs should be immediately thought of for the treatment of HIT after discontinuing the offending agent? What can be used for reversal of these agents if anticoagulation is too much?

A

Direct thrombin inhibitors, i.e. bivalirudin, argatroban, dabigatran

Dabigatran has a reversal agent monoclonal antibody, but the other two you must stop the bleeding somehow:

  1. Anti-tPA’s / antifibrinolytics: tranexamic acid, aminocaproic acid
  2. Prothrombin complex concentrate
164
Q

What is dual antiplatelet therapy and what are three indications?

A

Aspirin (anti-TXA2) and ADP receptor blocker (i.e. clopidogrel)

  1. Acute coronary syndromes - broken heart strings
  2. Prevention of coronary stent thrombosis - think of Sammy Sosa corked bats
  3. Ischemic stroke - think of black paint on painter’s head, also seen in statins sketchy
165
Q

What are the two phosphodiesterase inhibitors used to impair platelet activation and their mechanism of action?

A

Dipyridamole - Two pyramids on tent
Cilostazole - He lost the ball!

increased cAMP will impair platelet aggregation (i.e. TXA2 is meant to decrease cAMP synthesis), also causes vasodilation

166
Q

What can be used for reversal of thrombolytic therapy?

A

Competitive inhibitors of plasminogen - tranexamic acid (exam) or aminocaproic acid (capping paint)

FFP - fighter plane
Crypoprecipitate - the cap that the kid is wearing

167
Q

What is the difference in indication between cytarabine and gemcitabine?

A

Cytarabine - think of the archers in the cave next to the saber tooth tiger - only good for hematologic malignancies

Gemcitabine - think of the crabs on the gem rocks -> also decent against solid malignancies

Capecitabine is the prodrug of 5-FU

168
Q

What are the indications for actinomycin D?

A

Think of the actinomycin Doll -> childhood malignancies

Especially effective against Wilms tumor, Ewing sarcoma, and rhabdomyosarcoma

169
Q

What side effect is thought to occur most commonly with chimeric antibodies (i.e. rituximab, cetuximab)?

A

Serum sickness -> 7-10 days later, a type 3 hypersensitivity with arthralgias, fever, and rash due to deposition of immune complexes formed when we make antibodies vs the chimeric antigens in the monoclonal antibodies.
-> think of the guy with the crown dropping his cup

acute infusion reactions are also common if the injected antibody directly interacts with our lymphocytes -> pruritis and hypotension, fvers

170
Q

What are the side effects of cetuximab?

A

Rash - similar to Erlotinib (due to activity against EGFR in skin)

Infusion reactions and serum sickness can occur, as would be expected

171
Q

What is the ideal anticoagulant treatment for women, given pregnancy is a hypercoagulable state?

A

LMWH’s - which require minimal routine laboratory monitoring and have a long halflife

Switch to UFH at term -> shorter halflife, can be stopped rapidly at labor to prevent hemorrhage

Direct thrombin inhibitors and Xa inhibitors are CONTRAINDICATED due to pregnancy risk #1194

172
Q

What are the clinical manifestations of ARPKD and what is the function of the missing protein? When does it present?

A

Missing protein = polyDUCTin - another nonmotile cilia syndrome

Presents in infancy, often prenatally
-> associated congenital hepatic fibrosis leading to portal hypertension
-> renal failure and hypertension.
Think “Cysts in the liver, cysts in the kidney”

173
Q

What happens to the serum BUN/Cr ratio in intrarenal vs extrarenal causes of ATN and why?

A

serum BUN/Cr ratios -> increases above 15 in extrarenal causes, as tubules try to preserve volume and are functioning properly, and BUN can be reabsorbed while Cr cannot. Think BUN is resorbed to preserve medullary gradient.

Ratio falls below 15 in intrarenal AKI (i.e. ATN) because tubules are not functioning properly in reabsorption of BUN.

174
Q

What is the drug-induced hypersensitivity cause of intrarenal azotemia called? What are the symptoms?

A

Acute interstitial nephritis (AIN / ATIN)
-> involvement of interstitium with WBCs and eosinophils causes an acute renal failure

Symptoms are oliguria, fever, and rash starting days after administering a drug.

note that 90% of intrarenal azotemia is due to ATN, which is NOT this.

175
Q

What are causes of renal papillary necrosis other than progression from AIN?

A

SAAD papa with papillary necrosis

Sickle cell disease / trait - damages vasa recta
Analgesic nephropathy - think of the kletes in sketchy
Acute Pyelonephritis - damages tubules
Diabetes mellitus - damages vasa recta

-> conditions reduce renal blood flow and induce coagulative necrosis

Presents with gross hematuria / flank pain due to loss of papillae into urine

176
Q

What is primary FSGS caused by, and what will happen to the glomeruli / ECM?

A

Idiopathic (we don’t bother to study diseases which primarily affect minorities)

  • > it is like really bad MCD -> nonselective proteinuria, effacement of foot processes
  • > damage to podocytes -> leakage of plasma proteins = hyalinosis
  • > hyalinosis -> increased ECM production = sclerosis

Patchy hyalinosis and sclerosis can be seen.

177
Q

Who is membranous nephropathy (also called membranous glomerulonephritis since it is the sister of membranoPROLIFERATIVE glomerulonephritis) common in and what causes the primary form? Is it immune-mediated?

A

Most common cause of nephrotic syndrome in Caucasian adults

Primary form is due to antibodies to the phospholipase A2 receptor

Caused by antibodies in all cases, so YES it is immune-mediated. However, we don’t get a lot of complement deposition so it is nephrotic rather than nephritic.

178
Q

What are the causes of secondary membranous nephropathy?

A
  1. Medications - NSAIDs, penicillamine (also causes of AIHA, antibody production)
  2. Infections - HBV, HCV, syphilis -> all things causing massive antibody production
  3. Malignancies - solid tumors put new Ags in circulation
  4. SLE - this is the nephrotic presentation of SLE (ANA-mediated antibody disease)
179
Q

What is MPGN, Type I caused by if it is primary or seconday? Where do things deposit?

A

Primary - idiopathic (all nephrotic syndromes can be idiopathic)

Secondary - related to SLE, or associated with HBV or HCV, other autoimmune conditions -> pretty much the same causes as membranous nephropathy

Subendothelial immune complex deposits

180
Q

What do DIF show for MPGN Type I vs Type II?

A

Type I - granular deposition of IgG, C3, C1q, and C4 in the glomerulus diffusely (all complement components, not just alternative)

Type II - C3 deposition would be prominent in GBM adjacent to dense deposits, and in mesangium. C3 nephritic factor is IgG but will not stain because the C3 is formed peripherally. Also C1q and C4 would not be present (classical pathway components)

181
Q

Where does amyloid tend to deposit in the kidney? How does this cause dysfunction?

A

In the mesangium, but can deposit anywhere

Causes dysfunction by compressing and decreasing luminal area of surrounding capillaries
-> causes a nephrotic syndrome

182
Q

Why do azotemia, oliguria, HTN, proteinuria, and edema happen in nephritic syndrome?

A

Reduction in GFR due to hypercellular inflammation blocking filtration
-> azotemia, oliguria, hypertension (sodium retention)

Glomerular membrane damage but not high enough GFR for massive proteinuria
-> RBCs lost, proteins not as much. Proteinuria -> edema from loss of oncotic pressure.

183
Q

What is seen on EM for PSGN and how does this differ from nephrotic syndrome in appearance?

A

Large, subepithelial deposits (below podocytes, like membranous glomerulonephropathy), which are LARGER and more interspersed, like humps (vs MGN where they are closer together and smaller).

Humps > domes in terms of size

184
Q

What is the pathogenesis of Berger disease? Include the type of cell which is most damaged.

A

Susceptible individuals increase IgA synthesis following infection (or with celiac disease or decreased IgA clearance in hepatobiliary diseases)

  • > increased polymeric IgA
  • > deposition in mesangium of glomeruli
  • > activation of alternative complement pathway with primary mesangial injury
185
Q

What is the inheritance of Alport syndrome, and what is the major defect?

A

X-linked, defect in Type IV collagen alpha chains

  • > defective assembly and dysfunction of the GBM
  • > thinning and splitting of BM

(vs Goodpasture you get antibodies to the noncollagenous domain of Type IV collagen)

186
Q

What special LM finding is seen most often with Types III and IV lupus glomerulonephritis and why?

A

Types III & IV are both commonly seen to have “wire looping” of capillaries
-> rigid thickening of glomerular capillary walls, especially due to subENDOthelial immune complex deposition.

Think “wire lupus”.

Can happen in other types as well, but less common.

-> remember that this can progress to a Type II RPGN.

187
Q

What causes cystinuria? When should you suspect this?

A

Autosomal recessive PCT cystine-reabsorbing transporter

Poor absorption of four amino acids:
COLA
Cystine
Ornithine
Lysine
Arginine
  • > Suspect when a child presents with Staghorn caliculi
  • > cyanide-nitroprusside test
188
Q

What two risks are associated with dialysis in CKD?

A
  1. Prediposes for the development of cysts within the shrunken kidneys (due to obstruction and compensatory hyperplasia, not well understood) -> Acquired Cystic Kidney Disease
  2. Renal Cell Carcinoma - increased risk of cancer in the setting of the hyperplasia of Acquired Cystic Kidney disease
189
Q

What paraneoplastic syndromes are most commonly associated with RCC?

A
  1. Polycythemia - due to production of EPO
  2. Cushing syndrome - due to ACTH secretion (like small cell lung cancer)
  3. Hypercalcemia - PTHrP
  4. Hypertension - increased renin production (like reninoma)
190
Q

What is the most common pediatric renal neoplasm, how does it present? What cells is it comprised of? Is it normally sporadic or genetic?

A

Wilms tumor (Nephroblastoma) - presents as hematuria and hypertension (renin secretion)

Triphasic - Comprised of blastemal (primitive mesenchyme), epithelial (primitive tubules and glomeruli), and developed mesenchymal (stromal cells)

Normally sporadic, but may be genetic in 10% of cases.

191
Q

What is the classic presentation of transitional cell carcinoma? Does it recur?

A

Usually seen in older adults, presents with PAINLESS hematuria (renal cell carcinoma typically presents with flank pain)

Since the risk factors have field effect, these tumors are often multifocal and frequently recur.
Flat -> early p53 mutations, early invasion, poor prognosis
Papillary -> low grade, slower to invade, better prognosis

192
Q

Can loop diuretics or thiazide diuretics cause an arthritis?

A

Yes! Both cause hyperuricemia -> gout.

This is because uric acid reabsorption is increased in low volume states.

193
Q

What is the triad of Behcet syndrome?

A
  1. Recurrent aphthous ulcers
  2. Genital ulcers
  3. Uveitis causing visual disturbances
    - > etiology is unknown, possibly immune complex vasculitis following viral insult
194
Q

What is a Warthin tumor and who gets it? Is it malignant?

A

Papillary Cystadenoma Lymphomatosum

Always arises in the parotid gland in male smokers

Malignant in 10%, bilateral in 10% (like pheochromocytoma)

195
Q

What is the most common cause of death in cirrhosis? How can you differentiate it from Mallory-Weiss syndrome?

A

Ruptured esophageal varices with associated coagulopathy due to liver dysfunction

Presents with painLESS hematemesis (vs Mallory-Weiss which is painful)

196
Q

What type of esophageal carcinoma is most common in the rest of the world and what are its risk factors? Where does it arise?

A

Squamous cell carcinoma, arises usually mid-esophagus but can be anywhere

RF: alcohol and tobacco smoking**, hot liquids and achalasia (irritation), caustic strictures with repeated injuries, Plummer-Vinson, etc

In the US it’s Adenocarcinoma secondary to Barrett esopaghus

197
Q

Where does the upper 1/3, middle 1/3, and lower 1/3 of the esophagus drain its lymph? Note that this is the pattern of spread of esophageal carcinoma.

A

Upper 1/3 - Deep cervical nodes (venous drainage via inferior thyroid vein to SVC)

Middle 1/3 - Mediastinal nodes

Lower 1/3 - Gastric and celiac nodes

Think neck, lung, stomach

198
Q

What is it called when a portion of bowel twists on its mesentery and where does it happen in adults? Children?

A

Volvulus -> happens in sigmoid colon in adults due to long mesentery
(coffee bean sign on X-ray)

Children -> happens in cecum, due to association with congenital malformations (i.e. Meckel’s, malrotation-> Ladd bands from cecum around duodenum are also seen)

199
Q

What malignancies is Celiac disease associated with?

A

T-cell lymphoma - due to lymph hyperplasia / inflammation (enteropathy-associated T-cell lymphoma)

Small intestinal adenocarcinoma (rare, associated with the crypt hyperplasia)

200
Q

What are the symptoms and complications of diverticulosis?

A

Usually asymptomatic or associated with mild left lower quadrant discomfort

Complications:
Diverticulitis -> left-sided appendicitis
Diverticular bleeding (painless hematochezia)
Fistulas -> transmural inflammation could form for instance a colovesical fistula -> presents with air / fecalith in urine

201
Q

What does high stress on the right side of the colon / cecum cause? How does it present?

A

Angiodysplasia - an ACQUIRED malformation of the mucosal / submucosal capillary bed -> tortuous dilation
-> due to periodic stress which caused venous distention

Presents as lower GI bleeding / hematochezia in an older adult

202
Q

Does a syndrome of Juvenile polyposis predispose to cancer?

A

Yes - the hamartomatous polyps arise everywhere (stomach, colon)

  • > actually have increased risk for cancer
  • > Autosomal dominant, still presents before age 5
203
Q

How can Gilbert syndrome and Crigler-Najjar Type II be treated?

A

Treated via phenobarbital - upregulate liver enzyme synthesis via enzyme induction properties
-> improves symptoms if some working allele is still available

204
Q

How does gastrin increase acid secretion by the parietal cells?

A

Activates CCK-B receptors in two places.

Major effect:
1. Enterochromaffin-like cells -> stink of the gastrin blower stimulating the bee-hive. Increases histamine release from ECL cells which stimulates H2 receptors to increase cAMP.

Minor effect:
2. Parietal cells - directly increases Gq signalling (along with M3 receptors) to increase stimulation of H+/K+ ATPase. Think of the gas tank connected to the lemonade maker.

-> makes sense b/c it binds CCK-B receptor on parietal cells -> CCK should signal thru a Gq mechanism since you want contraction

205
Q

What are exceptions where informed consent is not needed?

A
  1. Emergency
  2. Patient is incompetent legally / lacks decision making capacity
  3. Patient waives his right for consent
  4. Therapeutic privilege - decide to withhold information if it would harm them for a good reason. I.e. they are post MI and you don’t want to tell them they also have cancer (harms their autonomy for beneficence)
206
Q

What are the criteria for an adjustment disorder?

A

Emotional or behavioral symptoms in response to a stress occurring within 3 months of a stressor, which will not persist for more than 6 months after stress is removed. (>6 = generalized anxiety disorder)

Features for another psychiatric diagnosis are not present (i.e. depression)

207
Q

What drugs are used for maintenance treatment of bipolar?

A 
Atypical antipsychotics
Carbamazepine - mania / maintenance
Valproic Acid
Lamotrigine - depression / maintenance
Lithium
208
Q

What will skin biopsy of Dermatitis Herpitiformis show via H&E and direct immunofluorescence?

A

H&E - neutrophilic infiltrate of papillary dermal tips (vs. psoriasis which shows neutrophils in the stratum corneum).

DIF - granular IgA deposition
-> strong association with celiac disease

209
Q

What is a nodular melanoma and the prognosis?

A

Subtype with early vertical growth, poor prognosis. (Creates a nodule because they grow into the dermis and push the epidermis up).

Can be any color and rapidly evolving / bloody.

210
Q

How is SSSS distinct from SJS-TEN?

A

Basically SJS-TEN is the SSSS of bullous pemphigoid -> the separation is at the DEJ in SJS-TEN (deeper than SSSS).

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