Now I have everything needed. Here are complete cross questions with answers for every topic:
OSPE Cross Questions (Viva)
🔬 CROSS Q's on ESR
Q: What does ESR measure / what is the principle?
ESR measures the rate at which red blood cells settle in a tube over 1 hour. RBCs normally repel each other (negative charge). In infection/inflammation, fibrinogen and immunoglobulins coat RBCs, neutralize the charge, and cause rouleaux formation (stacking like coins), which increases the sedimentation rate.
Q: What are the causes of a HIGH ESR?
- Infections (TB, bacterial infections)
- Inflammatory conditions (Rheumatoid arthritis, SLE, vasculitis)
- Malignancy (multiple myeloma - most dramatically raised)
- Anemia (fewer RBCs settle slower, paradoxically raises ESR)
- Pregnancy
- Old age
Q: What are causes of a LOW (falsely low) ESR?
- Polycythemia (too many RBCs, resist rouleaux)
- Sickle cell disease (abnormal shape prevents rouleaux)
- Spherocytosis
- Congestive cardiac failure
- Hypofibrinogenemia
Q: What anticoagulant is used in ESR? Why not heparin?
Sodium citrate (3.8%) in a 4:1 ratio (blood:citrate). Heparin cannot be used because it alters the membrane zeta potential of RBCs and artificially increases the ESR, giving false results.
Q: What is the angle rule in ESR?
The tube must be perfectly vertical. Even a 3-degree tilt can accelerate the ESR by as much as 30% because plasma rises along the upper wall while RBCs settle along the lower wall, reducing resistance.
Q: What is the formula for the upper normal ESR?
- Men: Age / 2
- Women: (Age + 10) / 2
(Wills Eye Manual formula for practical use)
🦵 CROSS Q's on Knee Jerk (Patellar Reflex)
Q: What is the reflex arc of the knee jerk?
- Receptor: Muscle spindle (in quadriceps muscle)
- Afferent (sensory): Femoral nerve → dorsal root → L3, L4 spinal segments
- Synapse: In anterior horn of spinal cord (monosynaptic reflex)
- Efferent (motor): Anterior horn cell → femoral nerve → quadriceps
- Effector: Quadriceps contraction → knee extension
Q: What type of reflex is the knee jerk?
It is a monosynaptic stretch reflex (only one synapse between sensory and motor neuron). It is also a deep tendon reflex (DTR).
Q: When is the knee jerk absent?
In lower motor neuron lesion affecting L3/L4:
- Peripheral neuropathy (diabetic, GBS)
- Tabes dorsalis
- Poliomyelitis
- Direct femoral nerve damage
Q: When is the knee jerk exaggerated?
In upper motor neuron lesion (lesion above L3/L4):
- Stroke
- Multiple sclerosis
- Cervical myelopathy
- Spinal cord compression above L3
Q: What is clonus and when does it occur?
Clonus is a series of rhythmic involuntary contractions (5-7 Hz) in response to a sustained stretch stimulus. It occurs in UMN lesions due to hyperexcitability of alpha and gamma motor neurons from loss of supraspinal inhibition. (Adams & Victor's Neurology)
💉 CROSS Q's on Neutrophil
Q: What is the normal percentage of neutrophils in blood?
50-70% of total WBC count. Normal absolute count: 2,500 - 7,500 cells/µL.
Q: What are the granules in a neutrophil and their function?
- Primary (azurophilic) granules: Contain myeloperoxidase, lysozyme, elastase - kill bacteria
- Secondary (specific) granules: Contain lactoferrin, collagenase - help in inflammation
- Tertiary granules: Gelatinase - help in tissue invasion
Function: Phagocytosis + destruction of bacteria via reactive oxygen species (ROS) and anti-microbial peptides; also form NETs (Neutrophil Extracellular Traps). (Firestein & Kelley's Rheumatology)
Q: What is neutrophilia vs neutropenia?
- Neutrophilia: >7,500/µL - seen in bacterial infections, stress, steroids, burns
- Neutropenia: <2,500/µL - seen in viral infections, SLE, chemotherapy, aplastic anemia
Q: What is a "left shift"?
Increased release of immature neutrophils (band cells, metamyelocytes) into the blood, indicating a severe or overwhelming infection where the bone marrow is pushed to its limit.
Q: How do you distinguish a neutrophil from an eosinophil on a blood film?
- Neutrophil: Pale pink cytoplasm, fine granules, multilobed nucleus (2-5 lobes)
- Eosinophil: Bright orange-red large granules, bilobed nucleus (classically 2 lobes)
🩸 CROSS Q's on Ovulation
Q: What hormone triggers ovulation?
The LH surge (Luteinizing Hormone). A sudden peak in LH (caused by high estrogen positive feedback on the anterior pituitary) triggers ovulation 24-36 hours later. (Berek & Novak's Gynecology)
Q: How does progesterone help confirm ovulation has occurred?
After ovulation, the corpus luteum secretes progesterone. A serum progesterone level >3 ng/mL on day 21 (mid-luteal phase) is presumptive evidence ovulation occurred. Progesterone also raises the basal body temperature by ~0.3-0.5°C. (Costanzo Physiology)
Q: What happens to cervical mucus at the time of ovulation?
Just before and at ovulation, estradiol causes cervical mucus to become:
- More abundant
- Watery and clear
- Highly stretchy (spinnbarkeit)
- Penetrable by sperm
After ovulation, progesterone makes it thick, scanty, and hostile to sperm.
Q: What is the constant phase of the menstrual cycle?
The luteal phase is always 14 days, regardless of cycle length. The follicular phase is variable. So in a 35-day cycle, ovulation is on day 21; in a 24-day cycle, it's day 10.
Q: What is the hormone sequence leading to ovulation?
FSH → Follicle growth → ↑ Estradiol → Positive feedback → LH surge → Ovulation (day 14) → Corpus luteum → ↑ Progesterone + Estradiol (luteal phase)
⚡ CROSS Q's on UMNL vs LMNL
Q: Why is there hyperreflexia in UMNL?
Upper motor neurons normally inhibit the spinal reflex arc. When this inhibitory control is lost (due to cortical/spinal cord damage), the lower motor neurons become disinhibited and hyperresponsive, resulting in exaggerated reflexes and increased tone (spasticity).
Q: Why is tone DECREASED in LMNL but INCREASED in UMNL?
- In LMNL: the motor neuron itself is damaged → muscle receives no signal → flaccid, hypotonic
- In UMNL: the inhibitory descending control is removed → spinal circuits are over-active → spastic, hypertonic
Q: What is the Babinski sign? What does it indicate?
Elicited by stroking the lateral plantar surface of the foot from heel to ball.
- Normal (negative): Flexion (plantar flexion) of toes
- Babinski positive: Extension (dorsiflexion) of great toe + fanning of other toes
- Significance: Indicates UMNL / corticospinal tract damage at any level
- Normal in infants under 1 year (myelination incomplete) (Adams & Victor's Neurology)
Q: In acute UMNL (e.g., right after a stroke), are reflexes increased or decreased?
Initially decreased / flaccid (spinal shock). Hyperreflexia and spasticity develop hours to weeks later as spinal circuits reorganize. (Neuroanatomy through Clinical Cases)
Q: Give 2 examples each of UMNL and LMNL
- UMNL: Stroke (internal capsule), Multiple sclerosis, cervical myelopathy
- LMNL: Guillain-Barré syndrome, diabetic peripheral neuropathy, poliomyelitis
❤️ CROSS Q's on Cardiac Output (HR = 72, CO = 5 L/min)
Q: What is the formula for Cardiac Output?
CO = Stroke Volume (SV) × Heart Rate (HR)
= 70 mL × 72 bpm = 5,040 mL/min ≈ 5 L/min
Q: What is Stroke Volume? What are its determinants?
SV = volume ejected per beat = EDV - ESV (~70 mL normally)
Three determinants:
- Preload - end-diastolic volume (Frank-Starling: more stretch → more force → more SV)
- Afterload - resistance the ventricle must overcome (↑ afterload → ↓ SV)
- Contractility - intrinsic ability of the myocardium to contract (independent of preload/afterload)
Q: What is the normal ejection fraction (EF)?
EF = SV / EDV × 100 = 70/120 × 100 ≈ 55-65%
EF < 40% = systolic heart failure
Q: If HR increases to 150, will CO necessarily increase?
Not always. At very high HRs, diastolic filling time decreases, reducing EDV and SV. So CO may actually decrease at extremely high heart rates (e.g., tachyarrhythmias).
Q: What is the Frank-Starling law?
The greater the end-diastolic volume (preload), the greater the stroke volume - up to a physiological limit. This is because more myocardial stretching leads to greater force of contraction (more actin-myosin overlap). (Costanzo Physiology, 7th Ed.)