EXTRA SLIDES INTEGRATED.pdf gtn is disease

Gtn

5. Hypertension
CategorySBPDBP
Normal<130<85
High-normal130-13985-89
Grade 1
hypertension
140-15990-99
Grade 2
hypertension
>160>100
Emergency: Severely elevated BP with acute
hypertension mediated organ damage (HMOD)
Urgency: Severely elevated BP without acute
hypertension mediated organ damage (HMOD)
Hypertension with:
DM / CKD/ Scleroderma-
Osteoporosis/ Renal stones-
Raynaud/ Cyclosporine induced-
BPH-
Migraine/ Thyrotoxicosis/ Angina/ Tremor-

6. vasoconstriction,aldosterone
secretion,renal sodium
retention, andsympathetic
nervous system activation.
Fetal, reproductive,
brain:Vasodilation, anti-
proliferation, apoptosis,
tissue repair

7. •The ECG shows:
•ST segment depressionin leads V1 to V3
•Tall, broad R wavesin V1–V3
•Upright T wavesin these leads

8. IntensityAtrovastatinRosuvastatinSimvastatinPravastatinLovastatin
High
(reduce LDL > 50 %)
40-80 mg20-40 mg-- -
Moderate
(reduce LDL by 30-49 %)
10-20 mg5-10 mg20-40 mg40-80 g40 mg
Low
(Reduce LDL by < 30 %)
--10 mg10-20 mg20 mg
High intensity statins indications:
•Clinical ASCVD/Acute Coronary Syndrome
•Prophylaxis for patients with history of Angina/myocardial infarction/stroke
•LDL > 190 mg/dl
•Hypertriglyceridemia with ASCVD risk

9. Poor PrognosisGood Prognosis
t(4;14), t(14;16), t(14;20), del(17p), aneuploidy,
hypodiploidyHyperdiploid,
↑ beta-2 macroglobulin t(11;14)
Plasmablastic morphologyt(6;14)
Low serum albumincyclin D1/D3+

10. Core Features of LBD
•Fluctuating cognition/alertness
•Recurrent, well-formed visual hallucinations
•REM sleep behavior disorder (RBD)
•Spontaneous Parkinsonism
Supportive and Associated Findings
•Autonomic dysfunction
•Depression, apathy, anxiety
•Dysphagia

11. 1.Systemic symptoms (fever, weight loss)
2.Systemic disease (cancer, HIV, immunosuppression)
3.Neurologic symptoms/signs (focal deficits, altered GCS, papilledema)
4.Onset sudden (thunderclap)
5.Onset after age 50
6.Pattern change (new or progressive)
7.Positional headache (worse lying vs standing → CSF leak, ICP)
8.Precipitated by Valsalva/exertion (cough, sneeze, exercise → raised ICP,
aneurysm)
9.Papilledema
10.Pregnancy / postpartum (risk of CVT, eclampsia, pituitary apoplexy)

13. Pseudobulbar
(UMN: 5,7,10,11,12)
Bulbar
(LMN: 9,10,11,12)
Gag reflex
Jaw jerk
Tongue
Speech Laboured/spasticNasal twang
Nasal regurgitation

14. Declarative / Explicit Memory:
•Semantic (factual):
•Prefrontal cortex
•Temporal cortex (lateral and anterior)
•Episodic (events):
•Hippocampus
•Medial temporal lobe
•Neocortex
Nondeclarative / Implicit Memory:
•Procedural (skills, habits):
•Striatum
•Cerebellum
•Motor cortex
•Priming and perceptual:
•Neocortex
•Associative learning (classical conditioning):
•Amygdala
•Cerebellum

15. MIGRAINE
First line:
DOC: 5HT1B/1D+ :
5HT1F + : LASMIDITAN (acute)

Prophylaxis:
Propranolol
Topiramate
Valproate
New drugs:
CGRP-: RimeGEPANT, AtoGEPANT
(oral-acute/prophylaxis)
ERENUMAB, GALANEZUMAB,
FREMANEZUMAB (monthly sc
injection),
EPTINEZUMAB (quarterly iv
infusion)
CLUSTER HEADACHE
DOC:
Prophylaxis:
TENSION HEADACHE
DOC:
Prophylaxis:

16. Cerebellar PartConnections & FunctionLesion Features
Flocculonodular lobe
(vestibulocerebellum)
Linked with vestibular nuclei,
maintains balance & eye
movements
Truncal ataxia, staggering gait,
nystagmus, positive Romberg
Anterior lobe (spinocerebellum)
Proprioceptive input from
spinal cord, regulates
posture & leg coordination
Gait ataxia, often in alcoholics
(anterior lobe syndrome)
VermisControls axial trunk musclesTruncal ataxia, broad-based gait
Dentate nucleus (lateral hemisphere /
cerebrocerebellum)
Coordinates planning &
initiation of voluntary
movement via
corticopontocerebellar
pathway
Dysmetria, intention tremor,
dysdiadochokinesia

18. Synucleinopathies:
•Parkinson’s disease
•Dementia with Lewy bodies
•Multiple system atrophy
Tauopathies:
•Alzheimer’s disease
•Progressive supranuclear palsy
•Corticobasal degeneration
•Pick’s disease
•Chronic traumatic encephalopathy
•Pantothenate kinase-associated degeneration
•Subacute sclerosing panencephalitis (SSPE)
•Down syndrome

20. FeatureGBS (AIDP)CIDP
OnsetAcute, monophasicInsidious, chronic/progressive
Progression≤ 4 weeks≥ 8–9 weeks
RelapsesRare, < 2≥ 3 relapses
TreatmentIVIG / PlasmapheresisSteroids, IVIG, plasmapheresis (long-term)

21. 91. Which of the following drugs act on sodium channels and
potentiate slow sodium inactivation?
A.Topiramate
B.Lacosamide
C.Phenytoin
D.Lamotrigine

22. Feature of RAMost common
Involved joints
Spine involvement
Extra-articular manifestation
Cardiac manifestation
Valvular abnormality
Pulmonary manifestation
Hematological manifestation
Ocular manifestation
Lymphoma
Cause of death

23. WHO analgesic ladder is a three-step approach for managing chronic pain:
Step 1: Non-opioids (e.g., paracetamol, NSAIDs) for mild pain.
Step 2: Weak opioids (e.g., codeine, tramadol) ± non-opioids for moderate pain.
Step 3: Strong opioids (e.g., morphine, fentanyl) ± non-opioids for severe pain.

24. •Hyponatremia:Serum sodium less than 135 mmol/L.
•Hypo-osmolality:Serum osmolality less than 275 mOsm/kg.
•Urine osmolality:Elevated above 100 mOsm/kg despite hyponatremia.
•Urine sodium concentration:Greater than 40 mmol/L with normal salt intake.
•Clinical euvolemia:No signs of volume depletion (no orthostatic hypotension, tachycardia, dry mucous
membranes) and no signs of fluid overload (no edema, ascites, or heart failure).
•Exclusion of other causes:Normal adrenal and thyroid function, no recent diuretic use, no renal failure,
and no conditions causing hypovolemia or hypervolemia.
•Correction with fluid restriction:Hyponatremia improves with fluid restriction.

25. •Type 1a:Most common; PTH resistance plus physical features of Albright Hereditary Osteodystrophy (AHO) (short
stature, round face, short fingers, subcutaneous ossifications).
•Type 1b:Mainly kidney PTH resistance without AHO phenotype.
•Type 1c:Similar to 1a but normal Gs alpha activity.
•Type 2:Normal cAMP response but impaired phosphate excretion

27. Interpretation
•Low probability: ≤0 points
•Moderate probability: 1-2 points
•High probability: ≥3 points
•PE unlikely: ≤4 points
•PE likely: >4 points

33. Uremia:
Pericarditis
P.Edema
Ph <7.2
Potassium >6.5
Encephalopathy
Bleeding diathesis

34. Dopamine
ANP
cAMP
PGE2

36. •Increased risk of cancers:
•Colon
•Stomach
•Small intestine
•Pancreas
•Breast
•Ovary
Distinctive PJ Tumors
•Sex cord tumor with annular tubules of ovary
•Large cell calcifying Sertoli tumor of testis
•Adenoma malignum of cervix

37. Diagnostic Criteria of Hepatorenal Syndrome
•Cirrhosis with Ascites
•Diagnosis of AKI
•No or inefficient response in 48 hours after diuretic withdrawal and adequate volume
expansion with IV Albumin
•Absence of shock
•No evidence of recent use of nephrotoxic drugs
•Absence of intrinsic renal disease

38. TypeCysteine PatternExample LigandsCells Recruited
CCTwo adjacent cysteinesCCL2 (MCP-1), CCL5
(RANTES), CCL11 (Eotaxin)
Monocytes, T cells,
eosinophils
CXCTwo cysteines separated
by one
•CXCL8 (IL-8), CXCL10 (IP-
10), CXCL12 (SDF-1).
Neutrophils,
lymphocytes
CX3CTwo cysteines separated
by three•CX3CL1 (Fractalkine).Monocytes, T cells
C One pair, no other
conserved Cs
XCL1 and XCL2
(Lymphotactins)T cells

39. Langerhans cells
Kupffer cells
Microglia
Osteoclasts
CD71
PAS-diffuse
CD41,42,61CD13,33,117
MPO
CD14, 64
NSE
CD38,138
CD16, 56
TdT
PAS-dot-blot
CD19CD3
CD4CD8

40. Ig TypeHalf-lifeKey Features
IgG23 days- Appears late → chronic infection - Only Ig to cross placenta - 4
subclasses - Opsonization, complement fixation, neutralization
IgA6 days- Two types: Serum IgA & Secretory IgA (dimer) - Secretory IgA → mucosal
immunity
IgM5 days- Pentamer, highest molecular weight - Appears early → recent infection -
Intravascular only - Agglutination, hemolysis, opsonization
IgD2–8 days- Surface Ig on B cells - Acts as antigen recognition receptor
IgE1–5 days- Type I hypersensitivity - Heat-labile - Increased in helminthic infections

44. FeatureNecrosisApoptosis
Cell sizeEnlarged (swelling)Reduced (shrinkage)
NucleusPyknosis → karyorrhexis → karyolysisFragmentation into nucleosome-
sized fragments
Plasma membraneDisruptedIntact; altered lipid orientation
Cellular contentsEnzymatic digestion; may leakIntact; may be released in
apoptotic bodies
InflammationFrequentAbsent
RoleInvariably pathologic (cell injury)Often physiologic; may be
pathologic (DNA/protein damage)

45. Pro-apoptotic
Genes (BH1-3)
Anti-apoptotic
Genes
Apoptosis
Initiators/Sensors
BAK geneBCL-2 gene (most
important)BIM gene
BAX geneBCL-XL geneBAD gene
p53 geneMCL1 genePUMA gene
GlucocorticoidsSex (Love) steroidsNOXA gene

48. Physiological Changes at High Altitude
Respiratory Adaptations
•Increased Ventilation
•Renal Compensation: The kidneys compensate respiratory alkalosis by excreting bicarbonate over days, allowing sustained
hyperventilation.
Hematological Adaptations
•Polycythemia
•Increased 2,3-BPG
Cardiovascular Adaptations
Increased Heart Rate and Cardiac Output
Hypoxic Pulmonary Vasoconstriction
Increased Blood Pressure
Cellular and Metabolic Changes
Increased Capillary Density and Mitochondrial Efficiency: Enhances oxygen utilization in muscles.
Upregulation of Hypoxia-Inducible Factors (HIFs): Modulates gene expression to adapt to low oxygen.
Other Effects
Sleep Disturbances: Due to periodic breathing and hypoxia.
Increased Cerebral Blood Flow: To maintain brain oxygenation but may contribute to high-altitude cerebral edema.
Muscle Atrophy and Weight Loss: Due to metabolic adjustments and reduced appetite.

51. Coupling ratio: 3:2
Stimulated-Thyroid, insulin, Aldosterone

52. ComponentSourceBehavior
Active tensionActin-myosin interactionMaximal at optimal length
(~100%)
Passive tensionElastic connective tissuesRises after the muscle is
stretched
Total tensionActive + PassiveComposite of both

53. NeurotransmitterReceptor Type
Glutamate-Ligand-gated ion channels: NMDA, AMPA
GABA- Ligand-gated: GABA A, GABA C
Acetylcholine-Nicotinic → Ligand-gated
Norepinephrine, 5HT,
Dopamine, AchM
GABA-B
GLycine
GPCR (except 5HT3 which is ligand-gated)

54. StructureFunction
Nociceptors (Aδ, C fibers)Detect noxious stimuli (thermal, mechanical, chemical)
Dorsal horn (Lamina I, II – substantia gelatinosa)First synapse; neurotransmitters: glutamate, substance P
Second-order neuronsCross midline (anterior white commissure) → ascend in
spinothalamic tract
Thalamus (VPL nucleus)Relay to cortex
Somatosensory cortex (S1)Conscious perception of pain
StructureFunction / Neurotransmitter
Prefrontal cortex, ACCModulates perception & emotional response
Periaqueductal gray (PAG)Activates descending inhibition pathways
Nucleus raphe magnusReleases serotonin → inhibits pain at spinal level
Locus ceruleusReleases norepinephrine → inhibits pain
Interneurons in dorsal hornRelease enkephalins, dynorphins → inhibit 1st/2nd order
synapse

55. The drugs which are secreted in bile and safe in renal disease include:
Cef in: Cefoperazone, Ceftriaxone
The: Tigecycline
R: Rifampicin
E: Erythromycin
N: Nafcillin
A: Ampicillin
L: Lincosamide (Clindamycin)
D: Doxycycline

56. Pathology/PatternCausative Agent
Cholestatic pattern Contraceptive and anabolic steroids
Spotty hepatocyte necrosisMethyldopa, phenytoin
Massive necrosisAcetaminophen, halothane
Chronic hepatitisIsoniazid
Microvesicular steatosisValproate, tetracycline, aspirin (Reye syndrome), ART
Fibrosis and cirrhosisAlcohol, methotrexate, enalapril, vitamin A
Noncaseating epithelioid granulomasSulfonamides, amiodarone, isoniazid
Fibrin ring granulomasAllopurinol