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U world Composite > Third 50 > Flashcards

Third 50 Flashcards

1
Q

Gastric Acid Secretion Mechanisms

A

-Parietal cell secretes it..Found in mucosal glands of the fundus and the body. Triggered by
1) Acetylcholine- M3 receptors- Ca release
2) Histamine-released by ECL- H2 receptors increased cAMP
3) Gastrin- GR on parietal cells, increased Ca. Also increases histamine synthesis and release by ECL (MOST IMPORTANT action)
Ca and cAMP activate PKinases, hence increased H/KL ATPASE

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2
Q

Mastocytosis, describe, GI observations

A

Cramps and Increased mast cells in mucosa..non GI related are pruritus, urcticaria, dermatographism, rash, flush

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3
Q

Gastric paresis or hypomotility

A

Hypothyroidism, uremia, DM, metabolic disturbances

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4
Q

Triple test? (pregnancy)

A
  1. AFP:- made by fetal liver, GI tract and yolk sac in early gestation. Maternal serum level increases with increased gestational age. Most common cause for increased levels is dating error (gestational age underestimated!!!! Other causes are neural tube defects, abdominal wall (omphalocele/gastroschisis) and multiple gestation..Downs syndrome = decreased AFP
  2. Estriol:- reflect placenta and fetal function…if decreased , placental insuffiency
  3. HCG:- made by trophoblastic tissue..increased levels correlate with multiple gestation, hydatidiform mole and choriocarcinoma
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5
Q

Use of Nitrates and paradoxical effect..solution? Is nifedipine helpful

A

Used in stable angina..
It is a vasodilator that decreases blood pressure
However, reflex tachycardia ensues, which increases myocardial o2 demand even though they are anti ischemic drugs…Use metoprolol or beta blockers to slow AV node conduction at beta1 receptor sites

NIFEDIPINE is a peripheral CaCB and can cause reflex tachycardia! Cardioselective CCB like Verapimil or diliatezem are better!!! They slow AV nodal conduction but beta blockers more effectively blunt the tachycardic response induced by nitrates

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6
Q

Name one alpha agonist and an antagonist and describe their function..do any of them cause reflex tachycardia…Describe hydralazine does it cause reflex tachycardia?

A

Agonist:- Phenylephrine, used as a vasopressor in shock cases or severe hypotension cases. Causes reflex BRADY as it is a POTENT vasoconstrictor
Antagonist:- Prazosin is a selective alpha 1..use in HTN and BPH. Peripheral vasodilator…Selective alpha blockers DO NOT cause reflex tachy as PRESYNAPTIC alpha 2 inhibition is not blocked

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7
Q

Name one alpha agonist and an antagonist and describe their function..do any of them cause reflex tachycardia…Describe hydralazine does it cause reflex tachycardia?

A

Agonist:- Phenylephrine, used as a vasopressor in shock cases or severe hypotension cases. Causes reflex BRADY as it is a POTENT vasoconstrictor
Antagonist:- Prazosin is a selective alpha 1..use in HTN and BPH. Peripheral vasodilator…Selective alpha blockers DO NOT cause reflex tachy as PRESYNAPTIC alpha 2 inhibition is not blocked

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8
Q

Where in respiratory tract is there ciliated mucosal epithelium..Function of Clara cells

A

NOSE to TERMINAL bronchioles lined by ciliated mucosal epitheliumn (BUT THERE ARE NO MUCOUS SECRETING CELLS WITHIN THE BRONCIOLES, EPITHELIAL CILIAL THERE DO OUTWARD CLEARANCE. SUBMUCOSAL MUCOUS AND MUCOSEROUS GLANDS FOUND IN OUTERMOST AIRWAY THROUGH BRONCHIA!!!!)
..MUCOCILIARY clearance ensures particles greater than 2 microns do NOT reach the alveoli…
They are non ciliated, found in terminal respiratory epithelium,,secrete clara cell secretory protein or CCSP which is part of surfactant, also detoxify inhaled toxins by cytP450..

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9
Q

What is responsible for HIV resistance to standard protease inhibitors
What encodes for structural glycoproteins

A

Pol gene mutations which are responsible for structural HIV RT changes making it resistant to standard NNRTs or NRT
HIV env gene encodes for the viral envelope glucoproteins which mutates to ensure humoral response resistant

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10
Q

Describe the structure of insulin and what drug increases insulin secretion and C peptide

A

N terminus is beta chain, then theres a C peptide and C terminus is A chain. A and B joined by disulfide bonds..C peptide cleaved from proinsulin by beta cell peptidases. bOTH ARE PACKAGED INTO SECRETORY GRANULES AND RELEASED IN EQUIMOLAR AMOUNTS!

Sulfonylureas increase insulin secretion and hence C peptide in type 2 diabetes

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11
Q

Two Bacillus anthracis virulence factors

A
  1. antiphagocytic polyD glutamic acid capsule
  2. anthrax exotoxin that is trimeric made up of protective antigen with translocates Edema factor (like Bordellas calmodulin dependent AC toxin) and lethal factor…PROTECTIVE FACTOR NEEDED for EF and LF to work
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12
Q

Centro versus Pan acinar Emphysema Pathogenesis

A

Centroacinar (heavy smoker with exertional dyspnea and airspace enlargement on CT):- oxidative injury to respiratory bronchioles, resident macrophages activated, recruitment of neutrophils to airspacem these realease MMP, proteinase 3, elastate, cathepsin G. Activated M’s release proteases…Neutrophils activated generated ROS which prevents alpha antitrypsin antiprotease. ..BUT ELASTASE in excess from neutrophils is KEY

Panacinar:- Usually due to alpha 1 antitrypsin activity- the major neutrophil elastase inhibitor

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13
Q

Histological changes in respiratory tract

A

Bronchi:- Pseudostratified columnar ciliated, goblet cells, submucosal mucoserous glands and cartilage.
Bronchioles, terminal bronchioles and respiratory brionchioles lack goblet cells, glands and cartilage
Terminal Bronchioles level:- Ciliated simple cuboidal
Epithelial Cilia persist to the end or respiratory bronchioles

Submucosal mucous and serous glands travel in cartilaginous plates in the tracheobronchial tree and end at the smallest bronchi

-BRONCHIOLES LACK GOBLET CELLS, GLANDS and CARTILAGE GENERALLY

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14
Q

Histological changes in respiratory tract

A

Bronchi:- Pseudostratified columnar ciliated, goblet cells, submucosal mucoserous glands and cartilage.
Bronchioles, terminal bronchioles and respiratory brionchioles lack goblet cells, glands and cartilage
Terminal Bronchioles level:- Ciliated simple cuboidal
Epithelial Cilia persist to the end or respiratory bronchioles

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15
Q

Atheromas

A

Plaque with a fibrous cap that undergoes remodelling
Keeps it stable
Activated macrophages can make MMPs to degrade collagen
Intimal inflammation can destabilize plaques leading to rupture, acute coronary syndrome and MI

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16
Q

Female Gamatogenesis

A
  • Starts at 4 weeks gestation (primordial germ cells migrate from yolk sac to gonadal region)
  • Differentiate into oogonia (46, 2N) then start meiosis I
  • Meiosis 1, primary oocytes (46, 4N), arrested in meiosis 1 until puberty
  • By 5 months all oocytes formed. Degenerate throughout life to menopause
  • With FSH at puberty, oocytes stimulated to complete meiosis 1
  • Secondary oocytes formed with polar bodies (23, 2N)
  • Secondary stats meiosis II, polar body degenerates. Halts in metaphase II
  • By Day 14, secondary released due to paradoxical LH surge from high estrogen.
  • Secondary frozen in metaphase of meiosis II until fertilization
  • With fertilization divides into mature oocyte and second polar body
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17
Q

Diabetes Complications two pathways

A
  1. Advanced glycosylation end products:- glucose attaches to amino acid residues, accumulate and becomes irreversible. Attaches to collagen, blood vessel, tissues leading to microangiopathy and nephropathy. This facilitates inflammation and LDL deposits hence atherosclerosis
  2. Polyol pathway in tissues that dont depend on insulin for glucose transport (kidney, peripheral nerve, lens, blood vessels). GLucose- sorbitol (aldose reductase)- fructose..High osmotic pressure, hence injury, in lens opacification and cataracts, in schwann cells, peripheral neuropathy
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18
Q

Holiday Heart Syndrome

A

Binge drinking can lead to palpitations (subjective awareness of heart beating), AFib:- irregularly irregular tachy (QRS, absent p waves), pericarditis, increased sympathetic tone

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19
Q

Cytokines, and chemotactic factors

-Neutrophils

A

NEUTROPHILS

  • IL8 is pro neutrophils and C5a is pro every wbc type while C3a is ONLY EOSINOPHILS AND BASOPHILS
  • LTB4 and 5HETE are also pro neutrophil

OTHERS

  • IL10 is anti inflammatory
  • IL3 secreted by active t cells leads to bone marrow cell differentiation
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20
Q

LEPTIN

A

Enhances satiety. HOW
- Increases POMC, this gets cleaved to aMSH which decreases eating
-Decreases NPY4 which makes you eat
These substances are made in the arcuate nucleus of the hypothalamus

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21
Q

Schizosss

-Distinguish schizophreniform from schizoaffective

A

Schizophrenia Symptoms are
Psychosis (Hallucinations, Deluisions, Disorganized Speech) and NEGATIVE SYMPTOMS. Need 2

If Schizophreniform, need 2 or more of schizophrenic symptoms plus 1-6 months of episodes…rarely mania
If Schizoaffective need PROMINENT mood symptoms in addition to schizophrenic symptoms. Also need 2 wks of psychosis in absence of mood

22
Q

Narcolepsy Drug

A

First line is Modafinil, a stimulant which is thought to act via dopamine
Second line is Amphetamines but due to increased sympathomimetic effects are not used as often

23
Q

Zolpidem

A

A non-benzo anti insomnia drug

24
Q

Tibial Nerve

A

Plantar flexion

Plantar foot/sole of foot sensation

25
Q

Kidney Metabolic Compensation Timeline

  • How does overuse of diuretics present
  • What about heroin
A

Timeline is 3-5 days
Diuretics abuse can lead to contraction alkalosis, hence aldosterone secretion, hence proton loss hence alkalosis
Heroin overuse leads to respiratory depression which acutely causes respiratory acidosis, later compensated with bicarb (initially bicarb is low)

26
Q

Mode of action of benzos vs barbiturates

A

Benzo’s increase the frequency of GABA channel opening while Barbiturates increase the duration of opening

27
Q

Anatomy of the abdomen,

  • where does the aorta bifurcate
  • What does the ileum resemble on CT
  • which renal vein drains the gonadal vein
  • Describe the pathway of the renal vein
  • What can be mistaken for IVC on CT
  • At what level can we see both kidneys
A
  • Aorta bifurcates at L4
  • Ileum looks like an 8
  • On the left the left gonadal vein drains into the left renal vein
  • Renal vein goes anterior to the aorta but posterior to the SMA then drain in the IVC
  • Dont mistake duodenum for IVC,. IVC is next to the aorta right in front of vertebral bodies
  • L2 is the level at which both kidneys can be imaged
28
Q

Increased ACTH has whhat effect on the kidney

A

HYPERPLASIA not hypertrophy of both the Fasiculate (Cortisol) and Reticulata (sex hormones_

29
Q

Trisomy 18

A

AKA Edwards

  • Microcephaly
  • Low set ears
  • Small mandible
  • Fist clenched
30
Q

Which lifestyle modification is tantamount

A

SMOKING CESSATION

31
Q

COngenital bicuspid aortic valves

A

sixth decade calcific aortic stenosis!!!

These tend to be asympathomatic, no murmors or outflow tract issues, in contrast to congenital aortic stenosis!!!!

32
Q

Hepatitis B antigens

A
  • s Ag comes up first, before symptoms and peaks when most ill, undetected in 3-6 months unless chronic phase
  • Shortly after HBsAg is HBeAg and HBV DNA:- active viral replication
  • (shortly before onset of symptoms, there is anti-HBcAg and increased serum transaminases)
  • anti-HBcAg IgM is replaced with IgG OVER next months
  • anti-HBeAg appears after HBeAg vanishes hence transtion from high viral replication and infectivity to lower.
  • Anti HBsAg IgG rises post resolution of acute phase UNLESS chronic phase
33
Q

Pituitary Apoplexy

A

Acute bleed into pituitary adenoma

  • Sudden headache and cranial nerve paralysis. Signs of meningeal irritation
  • CV collapse if adrenocortical crisis

Same as berry aneurysm rupture EXCEPT visual field pituitary apoplexy

34
Q

Sheehans

A

Postpartum women

  • Ischemic necrosis of the pituitary
  • Indolent
  • Failure to lactate
35
Q

Aortic Stenosis sounds, causes

A

Cres-Decrescendo
Systolic ejection
Right sternal border
-Exertion/Syncopie

-Causes
Congenital abnormal valve with calcification (e.g. bicuspid aortic valve, calcified normal valve (more common US), rheumatic heart disease (more common worldwide)

36
Q

Lynch Syndrome

A

Hereditary non polyposis colon cancer. Autosomal dominant. Defective DNA mismatch repair

  • mutS (detects mismatch) and mutL (loads exonuclease 1) homologs. coded for by MSH2 and MLH1 involved in 90% mutations
  • Normal DNA polymerase proofreading still leads to errors every 10^6 base
37
Q

Samsters triad

A

-Asthma
-Aspirin hypersensitivity (nasal symptoms, , facial flushing bronchospasm )
-Nasal polyposis
Occurs in 10% of asthmatics treated with aspirin due to Leukotriene overproduction!!! (aspirin blocks COX!!!)

38
Q

High dose aspirin causes

A

Salicylism
-Vertigo
-Tinnitus
-Hearing loss
Can cause Hyperpnea via stimulation of respiratory drive hence
-respiratory alkalosis
-salicylate accumulation leading to metabolic acidosis

39
Q

Effect of steroids on liver, peripherally

A

Potent stimulators of liver glucooneogenesis., glycogenesis

  • Stimulate PEP carboxykinase
  • Glucose 6 phosphatase
  • Glycogen synthase (increased glycogen reserve in terms of stress)

Peripherally
-Antagonize insulin
-Favors catabolism (proteolysis and lipolysis)
Hence muscle weakness, skin thinnning, impaired wound healing, osteoporosis and immunesuppresion, hyperglycemia

40
Q

Cox 1 and 2 expression

A

COX 1 is constituitively expressed and 2 is undetectable except in activated inflammatory cells , hence is inducible and is 72kD

41
Q

Mycoplasma and Ureaplasma

A

LACK PEPTIDOGLYCAN CELL WALL
-RESISTANT TO AGENTS THAT ATTACK THE WALL
NO penicillins, cephs, vanc, carbapenems
USE ANTI RIBOSOMALS LIKE tetracycline and erythromycin

42
Q

Dilated CDM causes

A 
Viral myocarditis (Coxsackie B)
Peripartum cardiomyopathy
Alcohol
Chronic SVTs
Cardiotox drugs e.g. doxorubicin
Thiamine Deficiency (Wet beriberi)

IT IS A DIAGNOSIS OF EXCLUSION

43
Q

On what chromosomes are these tumor suppressor genes (diseases in bracket)

  • VHL
  • RB
  • NF-1
  • WT-1
  • BRCA-1
A 
VHL- 3 (RCC in 40% cases, cerebellar hemangioblastoma, Pheos!)
RB-13 (RB and osteosarcoma)
NF-1 -17 (NF-1)
WT-11 (Wilms tumor)
BRCA1- ovarian and breast
44
Q

Adenomatous polyps

  • Describe them histologically
  • Genetic changes
  • Malignant?
A

Dysplastic mucosa
Premalignant
>50 yrs old
Mutations in APC tumor suppresor
Stepwise progression to adenocarcinoma with mutations in KRAS, p53 and DCC
INCREASED COX2 activity in some forms of colon AC/inherited polyposes. HENCE ASPIRIN CAN LEAD TO LOWER INCIDENCE

45
Q

Ectoderm has three components

A
  • Surface Ectoderm
  • Neural Tube
  • Neural Crest
46
Q

What are derivatives of surface ectoderm

A
  • Rathkes pouch/anterior pituitary
  • Lens and cornea
  • Inner ear sensory organs
  • Olfactory epithelium
  • Nasal and oral epithelial linings
  • Epidermis
  • Salivary Gland
  • Sweat and mammary glands
47
Q

Neural Tube

A
  • Brain and spinal cord
  • Posterior Pituitary
  • Pineal Gland
  • Retina
48
Q

Neural Crest

A
  • A/P septum and endocardial cushions
  • Autonomic/Sensory/Celiac Ganglia
  • Schwann cells
  • Pia and arachnoid matter
  • Branchial arches (bones AND cartilage)
  • Skull bones
  • Melanocytes
  • Adrenal medulla
49
Q

Mesoderm

A
  • all 3 kinds of muscles
  • Connective tissue
  • Bone and cartilage
  • Serosa linings of peritoneum
  • cardiovascular system
  • Blood
  • Lymphatic system
  • Spleen
  • Internal Genitalia
  • Kidney and ureter
  • Adrenal cortex
50
Q

Endoderm

A 
GI tract
Liver
Pancreas
Lung
Thymus
Parathyroid
Follicular cells of thyroid
Middle ear
Bladder
Urethra
51
Q

T cell maturation

  • Where are the cells made
  • When and Where do they mature (what processes exactly happen here)
  • Where do positive and negative selection occur
A
  • Made in bone marrow and mature in thymus in FIRST trimester of gestation.
  • Thymus (TCR arrangement, positive and negative selection, extracellular markers and co-stim expression)
  • Come in negative
  • B chain of TCR expressed
  • Begin to be doubly positive
  • A chain expressed
  • Positive selection in thymus cortex and negative in medulla
  • Loss of either CD4 or CD8

U world Composite (4 decks)

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