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 Expired air: PO2 120 mmHg, PCO2 27 mmHg.

Dry inspired air: PO2 160 mmHg, PCO2 0 mmHg.

Humidified tracheal air: PO2 150 mmHg, PCO2

0 mmHg.

Alveolar air: PO2 100 mmHg, PCO2 40 mmHg.

Mixed venous blood: PO2 40 mmHg, PCO2 46

mmHg.

Systemic arterial blood: PO2 100 mmHg, PCO2

40 mmHg.

Partial pressures of gases in the lung:

FREE SAMPLE Join

Ventilation (V)

VD/VT ratio = 30 percent

@Mindmapfactorysamples
Anatomical dead space (ANDS) = 150 mL
Dead space volume (VD) = 150 mL
Alveolar dead space (ALDS) = 0 mL
Types of Dead Space
Total dead space = ANDS + ALDS Tidal volume (VT) = 500 mL

If ALDS is greater than 0, it is pathological.

4.2 L/min useful ventilation 350 x 12 VA/min = (VT-VR) x RR Alveolar ventilation volume (VR) = 350ml

1. Anatomical dead space: Single breath

nitrogen or Fowler’s method.

Telegram
VD = VT x (PaCO2 - PECO2) / PaCO2  Measurement of Dead Space

PaCO2 = Alveolar CO2 2. Physiological dead space: Bohr’s equation. 

PECO2 = Expired CO2

Tidal Volume and Dead Space

Alveolar Ventilation and Pulmonary
Pulmonary circulation (deoxygenated blood) = Circulation
Weibel model (23 airway generations):
5.5 L/min
Trachea Bronchi Bronchioles Terminal
Highly distensible. bronchioles (16th generation)

Low pressure. 23rd generation: Alveolar sacs Alveolar

ducts Respiratory bronchioles

First 16 generations: Conduct air, no gas

Conducting Airways
exchange (also called dead spaces).

Pseudostratified columnar ciliated epithelium:

Histology
Ciliary movement (using dynein) clears sputum.

Basal cells.
Stem Cells
Zonal Distribution of Blood Flow in the Lung 
Clara cells (Regeneration).

Exaggerated bronchoconstriction leads to

Contraction Bronchoconstriction
bronchial asthma.

Hypoxia closes oxygen-sensitive potassium Relaxation Bronchodilation.

channels.
Perfusion (Q) : pulmonary arterial pressure (Pa), pulmonary venous pressure (Pv)
This leads to potassium accumulation, causing gradients, pulmonary alveolar pressure (PA)
depolarization and opening of calcium channels.
Effect of Hypoxia
Resulting in vasoconstriction due to calcium Airway Smooth Muscle
influx.

This mechanism is unique to the lung.

Situs inversus: Improper rotation of internal

organs due to inadequate ciliary movement.
Note Absence of dynein leads to:
Asthenospermia: Immotile sperm.
V/Q Ratio in Different Lung Zones 

Kartagener syndrome (under immotile cilia

syndrome):
Ventilation-Perfusion (V/Q) Ratio
Last 7 generations are responsible for gas
Airway Generations exchange (also called exchange or respiratory
airways).

Shunt occurs when perfusion is present but

ventilation is absent, leading to conditions like
atelectasis.

Dead space occurs when ventilation is present

but perfusion is absent, as seen in pulmonary
embolism.

Ventilation-Perfusion Mismatch 

Pneumocytes 

Alveolar Airways

Composition 
Surfactant
Normal lecithin to sphingomyelin ratio is
Used to assess fetal lung maturity.
greater than or equal to 2.

Decreases surface tension to prevent alveolar

collapse.
Functions
Surfactant deficiency leads to alveolar
Treatment: Lucinactant.
collapse, causing hyaline membrane disease.

Regulation of Surfactant Production 

Respiratory
Inspiration affected. 1. Variable Extrathoracic Obstruction:
Physiology: Part 1
Expiration affected. 2. Variable Intrathoracic Obstruction:

Both inspiration and expiration affected. 3. Fixed Obstruction (Intra or Extrathoracic):

Cannot determine residual volume (RV),

functional residual capacity (FRC), or total lung Limitations of Spirometry Inspiration: Increased volume, decreased
capacity (TLC). pressure.
Pressure (P) is inversely proportional to Volume
Boyle's Law
(V).
Helium dilution technique: Used for FRC Expiration: Decreased volume, increased
measurement. pressure.

Nitrogen washout technique. Alternative Measuring Techniques

Body plethysmography: Most commonly used.

Intrapleural pressure (IPP)

FREE Alveolar Pressure (AP)

Transpulmonary Pressure (TP)

Changes during respiration.

Becomes negative during inspiration and

positive during expiration.

TP = AP - IPP (Intrapleural Pressure).

SAMPLE Join
@Mindmapfa
Types of Obstructive Diseases

Lung Pressures

Changes

Tidal Volume (TV): 500 mL

ctorysamples
Inspiratory Reserve Volume (IRV): 2-3 L

Expiratory Reserve Volume (ERV): 1.3 L

Mechanics of Breathing
Residual Volume (RV): 1.2 L

Functional Residual Capacity (FRC): 2.5 L

Telegram
Static Lung Volumes and Capacities

Difference between pressure-volume curves of

inspiration and expiration.

FEV = TLC - RV

FEV1: Volume of air expired in the first second.

Decreased in obstructive lung disease.

FEV1/FVC ratio:
Normal or increased in restrictive lung disease.

Hysteresis

Maximum during expiration.

C = ΔV (Change in volume) / ΔP (Change in

pressure).
Dynamic Lung Volumes

Spirometry Compliance (C)

No air-fluid interface.
Air expired from large airways (trachea and
AB segment (effort dependent): Saline-filled lung: No surface tension.
bronchi).

No hysteresis.
Air expired from medium and small airways.
BC segment (effort independent):
Affected in COPD. Lung Compliance

Air-Filled Lung vs Saline-Filled Lung

Effort Dependent and Effort Independent Segments

Volume at which opposing forces (expanding

and collapsing) reach equilibrium.
1. Equilibrium Volume
Occurs at functional residual capacity (FRC).

Volume of air remaining in the lungs after

complete lung collapse.
2. Minimal Volume
Seen in pneumothorax.

Effort independent portion affected.

Dog leg or ice cream scoop pattern:
Seen in COPD.

Lung vs Chest Wall vs Lung + Chest Wall

Emphysema leads to increased compliance.

Effect of Diseases on Lung Compliance
Fibrosis leads to decreased compliance.

Effect of Diseases
 Hypoglycemia

Confusion

Altered level of consciousness

Symptoms Seizures

Require prolonged monitoring Sulphonylureas Insulin/Insulin secretagogue Tremors

Drugs
Alcohol Sweating

Hepatic/renal/cardiac failure Symptoms consistent with hypoglycemia

Clinical Presentation
Sepsis Critical illness Diagnosis Whipple's Triad A low plasma glucose

Inanition Relief of symptoms after raising plasma

Etiology glucose
Cortisol
In clinical setting plasma glucose <70 is
GH Hormone Deficiency considered as hypoglycemia
Plasma Glucose = CBG x 1.11
Glucagon and Epinephrine CBG therefore approximately should be =
63 mg/dl for plasma glucose to be 70
non-Islet cell tumor mg/dl

Measure CBG < 70 go to step 2 ( as modern

Step 1 CBGs are calibrated to give plasma glucose
value )

Management Step 2

1-2 mg Subcutaneous/IM Glucagon in Diabetics Alternatives

Administer 25D rapidly IV or oral glucose

D5/DNS Slow IV Infusion

Step 3
Monitor CBG
 Shock

Fever
May not be seen in elderly, uremic, and Hypotension = MAP <60mmHg
Sepsis
alcoholics
Chills Tachycardia

Pancreatitis Clinical Features Pallor

Flat JV Distributive
Anaphylaxis Restlessness

Neurogenic Altered Sensorium

Endocrine Related

Pericardiac Tamponade Step 1 Check Vitals and Presentation

Massive PE Obstructive Urinary Catheter

Tension pneumothorax Airway Management - supplemental O2 SpO2 b/n 92-95%

History of Bleed or Trauma Consider central venous/pulmonary artery

Differential Diagnosis catheter
Burns
Hypovolemic Step 2 If in Shock Check for Volume Overload Arterial Line
Oliguria <20ml/hr is common in metabolic
DKA
acidosis
Polyuria
DI

MI Temporarily place in reverse trendelenberg

JV distension Cardiogenic position
Arrhythmic

JVD + Paradoxical Pulse Cardiac Tamponade

Initial Treatment
Murmurs Assess for HF

Infuse at 4 ml/hr rate using an infusion

pump

Present Noradrenaline - 1st line in distributive shock

Vasopressin - 2nd line

Volume Overload
4 ampoules Noradrenaline + 42 ml Normal
Saline/ Ringer's Lactate in a 50 ml syringe

Absent Give IV fluids Only If no response

Step 3
IV fluids via two green channels in both
Haemorrhagic Shock - Ongoing hands
haemorrhage
or Blood transfusion if possible

Cardiogenic Shock Dobutamine 2-20 ug/kg per minute

 Telegram Channel for daily medical content : @medtalkss00
Macule: Less than 1 cm in size

Patch: Greater than 1 cm in size

Flat lesions Macules and Patches
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premium channel, details on the channel @mindmapfactorysamples
-

Papule: Less than 1 cm

Raised lesions Papules and Plaques
Plaque: Greater than 1 cm

Collection of small skin lesions, some flat

(macules) and some raised (papules)
Maculopapular Rash
Largest organ in the body
Common in various disorders (e.g., drug rash, Morbilliform Rash
(looks like measles)
scarlet fever, syphilis, rubella)
Overview Barrier against infection
Vesicle: Less than 1 cm
Prevents water loss
Fluid-filled lesions (blisters) Vesicles and Bulla Lesion Types
Bulla (plural: Bullae): Greater than 1 cm

Pus-filled vesicle with a white center (e.g., acne, Epidermis: Keratinocytes (squamous epithelial
Pustule
pustular psoriasis) cells)

Smooth, elevated papule or plaque surrounded Layers of Skin Dermis: Connective tissue, vessels
by erythema (redness)
Type I HSR

Wheal Subcutaneous fat (also called hypodermis or

Often itchy, caused by dermal edema (seen in subcutis)
urticaria/allergic reactions)
-
Pale to Red
Blanch cli pressure
-

Peeling or flaking of the stratum corneum (e.g.,

Scale Stratum Basalis: Stem cells
psoriasis)

Dried exudate of a skin lesion (e.g., impetigo) Crust Stratum Spinosum: Desmosomes form spines

Skin Epidermal Layers

Stratum Granulosum: Keratohyalin granules
form keratin filaments
Directly caused by the disease process
Primary Lesions Stratum Lucidum: Clear layer of dead skin cells
Described using standard terminology (e.g.,
macules, papules, vesicles, bulla) Stratum Corneum: Anucleated cells filled with
Skin Lesions keratin filaments
Modifications of primary lesions, or caused by
trauma/external factors
Secondary Lesions
Examples: Scale, crust, erosion, fissure, ulcer Connective tissue
Dermis
Blood vessels

Hyperpigmented (dark) plaques on the skin

Psoriasis
Eg
Commonly occurs in intertriginous areas Hyperkeratosis: Thickening of the stratum Callus

corneum, excess keratin (geiten player)

(folds), such as the neck and axillae
Acanthosis Nigricans Parakeratosis: Hyperkeratosis with retained
Psoriasis &
Associated with hyperkeratosis and mild skin
malignancies
acanthosis nuclei in the stratum corneum, indicating
hyperproliferation
Often linked to insulin resistance, and rarely,
malignancy Gastric Adenocarcinoma Hypergranulosis: Increased thickness of the
stratum granulosum, seen in lichen planus
---
=> - - -

Used to describe microscopic findings in skin

Dermatopathology Terms biopsies Spongiosis: Fluid accumulation (edema) in the
epidermis, seen in eczema and other skin
disorders
:Y
-
unded Acantholysis: Loss of connections between
Keratinocytes
.
freely floating keratinocytes, often due to loss of
desmosomes, seen in pemphigus vulgaris

/
Acanthosis: Diffuse epidermal hyperplasia with
- elongated rete ridges and thickening of the
M spinous layer
 Male reproductive hormones include
testosterone, dihydrotestosterone (DHT), and
androstenedione.
A dilatation of the pampiniform plexus of the Overview
spermatic veins, usually occurring on the left These hormones are crucial for the
side. Isolated
+
Sided
-
Right> ↑ Suspicion for RCC development of male reproductive organs and
Harmaturia secondary sexual characteristics.
Associated with scrotal pain, swelling, and
possible infertility due to increased testicular Varicocele
temperature.
B/L
Cryptorchidism
Produced by the Leydig cells in the testes and
varicocelectomy Male
Phenotype +

Treatment includes surgery or embolization to adrenal cortex.

(
Danger
redirect blood flow from the dilated veins.
Cause
Testis be
CA It may
absent
I exposed
to ↑
I - Cholesterol is the precursor of testosterone.
usingosant Androgens

AMPSee
clot off
↓ Agenesis
the veins Ambiguous genitali
male
may appear

& Testosterone is responsible for the

wli Absent testis

The condition of undescended testes, which ↓

shock
Serum
development of internal male genitalia, such as
Testosterone
Risk of

may be located in the abdomen or inguinal from low

Cortisol
Testing Cholesterol

the seminal vesicles, epididymis, and vas

↓
canal. ↑ Temp
Exposed to DX-ACTH,
Cortisol ↑ CH/FSH ,
absence
Also-made
by
Adrenal Cortex
DHEA Androstene
dione
-

deferens.
but can't make
of MIH
testosterone

Testosterone

Complications include low sperm count, Some testosterone effects are mediated
increased risk of germ cell tumors, and Cryptorchidism through conversion to dihydrotestosterone

·
testicular torsion. (DHT) and estradiol.

u
Treatment involves surgical placement of the Testosterone is converted to DHT in peripheral
testes in the scrotum (orchiopexy). Temperature Effects
tissues by the enzyme 5-α reductase.
Done after 6months
Leydig
is
Sertoli is
Less Sensitive
Sensitive
(4 Temp) ~
DHT has increased potency and binds to the
Sertoli cells support and nourish developing I Testoster one

production is
androgen receptor more strongly than
sperm and regulate spermatogenesis.
↓ spermatogene is ↓ inhibin B
↓
maintained at testosterone.
↑ Temp
↑ FSH
Key Hormones Dihydrotestosterone (DHT)
They form the blood-testis barrier, secrete DHT is more stable and is responsible for the Derived
inhibin B (which inhibits FSH), and produce development of external male genitalia, such as from
Intra-testicular androgen-binding protein to maintain high local Sertoli Cells the penis and scrotum. prostate bladder
, , Urogenital
testosterone conc. Sinus
testosterone levels. stimulated
by FSH from
100Xhighe
is p
pituitary
a

↓
Finasteride inhibits 5-α reductase and is used to
This is
why doesn't
exogenous Sertoli cells also secrete anti-Mullerian Supportedby Leydigea treat benign prostatic hyperplasia (BPH) and
testosterone
Work hormone during fetal development, leading to :. Both CH & FSH are needed
hair loss.
spermatogenes
is
for
the degeneration of the Mullerian ducts.
Join Telegram Testosterone is also converted to estradiol by

Male Reproductive @medtalkss00 for

the enzyme aromatase, which is present in
adipose tissue and Leydig and Sertoli cells.
A potassium-sparing diuretic that blocks
Other
Drug aldosterone receptors. Hormones more. And Instagram Estradiol (17β-estradiol)
Some effects of testosterone are mediated by
@mindmap_factory
·

Ketokonazole

estradiol, especially in regulating bone growth

·

Cimetidine
5 X Reductase
-

inhibitors
·

CCB It also blocks androgen receptors and reduces and closure of epiphyseal plates during puberty.
Omerprazole
androgen production, leading to increased Spironolactone
·

·
2nd Gen .
Antipsychotics

↑ estrogen effects. from androstenedione

<
Gynaecomastia
(Rey SE)
·
-

↓ Androgen effects
↓
is Used to treat conditions like acne, hirsutism, Stimulates progesterone The SRY gene on the Y chromosome produces
Alternative receptors
Eplerenone and androgenic alopecia in women. I testis-determining factor, leading to the
CNo gynaecomastial Blunts testosterone effects can cause Amenorrhea development of the testes.
↑ effects Fetal Development
Estrogen
Testosterone is required for the development of
High doses of androgens are sometimes used internal male genitalia, while DHT is required for
by athletes to increase muscle mass. external male genitalia.
Anabolic Steroids
Adverse effects include decreased HDL, Testosterone leads to the enlargement of the
Acue >
- d/ + ↑ Sebum

increased LDL, erythrocytosis, testicular to estrogen scrotum and testes, growth of the penis, and
↑
Androgen &
↓
Puberty
Exogenous Androgen
atrophy, azoospermia, and gynecomastia. Alter SHBG
the development of secondary sexual
Secretion
↑
ofSebaceous

of steroids the glands + ↑

- dIt -
BIn
tests
closes
can't recover & characteristics, such as pubic hair, facial hair, growth
↑ EPO ↑ Iron Utilization ↑

In blu closes there is excess

and deepening of the voice. androgenogen -
PLOS

estrogen Effects of Testosterone Puberty

excess) CAH

Spermatogenesis is regulated by testosterone

produced by Leydig cells and supported by => Estrogen (converted from testosterone) is
Sertoli cells. responsible for the growth spurt and closure of
epiphyseal plates. ↑ Linean
growth
Spermatogenesis
Exogenous testosterone can suppress LH
~ secretion, leading to decreased testosterone Testosterone continues to affect the prostate,
muscle mass, bone density, and red blood cell
on
weak effect production in the testes and reduced

spermatogenesis spermatogenesis. I Adult

production.
Ant Scalp

· It may contribute to conditions like benign &

Temporal
prostatic hyperplasia (BPH) and male pattern scalp

Used in male hypogonadism to increase muscle

=> baldness (androgenic alopecia). d/t androgens
Mid scalp

mainlyDHT Vertex

mass, bone density, and sexual function. Male +

ambiguous genitalia Testosterone tHDL & ↑LDL
Testosterone Therapy masculinization Exogenous Responds
Male
Hypogonadism
Female child +
to finasteride
Adverse effects include an increase in
at
puberty
hematocrit, acne, balding, and worsening of
Blind
vagina Autosomal recessive disorder where 46,XY
Absent uterus
males cannot convert testosterone to DHT.
BPH.
Maybeenquired
Conge
BIL Cryptorchidism
Normal Testosterone

Internal genitalia develop normally, but external

5-α Reductase Deficiency genitalia are female or ambiguous at birth.
Associated w/i
whi Aging
May
=
occur
↓ Sexual f(x)
·
Sn Testosterone
These individuals typically experience
↓ Bone Mass masculinization at puberty due to the effects
↑ SHBG ·

ANAENIA of increased testosterone.

↓ Free Testosterone
·
 Gonadal failure: Low testosterone with high LH.

Testosterone tumor: High testosterone with low

LH. In conditions like gonadal failure or exogenous
Male Development

·
testosterone use, LH and testosterone levels Hormonal Feedback in DSD
Exogenous testosterone: High testosterone with exhibit characteristic patterns:
low LH.
Chromosomal sex (XX/XY)

·
CAIS: High testosterone with high LH due to Disorders of Sexual Development (DSD) involve
androgen receptor resistance. Gonads (testes/ovaries)
a congenital discrepancy between:
of male factors in XX
presence
Absence of male factors in XY
External genitalia

Karyotype: Determines chromosomal sex (XX or Default genital development is female, with
XY). male development requiring testosterone,

t
Overview dihydrotestosterone (DHT), and Mullerian
Abdominal imaging: Identifies presence of inhibiting factor (MIH).
testes or uterus.
Key diagnostic test: Karyotype.
17-hydroxyprogesterone: Elevated in 21-
Diagnostic Tests for DSD

M
hydroxylase deficiency (CAH).

Testosterone and DHT: Both elevated in CAIS, Turner Syndrome (45 X): Affects females,
with reduced DHT in 5-α reductase deficiency. leading to short stature, lack of ovarian
development, and other physical abnormalities.
Luteinizing Hormone (LH): Varies based on
testosterone levels; increased in gonadal failure Klinefelter Syndrome (47 XXY): Males with an
or androgen resistance. Sex Chromosome Disorders extra X chromosome, leading to small testes,
infertility, tall stature, and learning disabilities.
of chromosomes
Aneuploidy
sex

Double Y Males (XYY): Normal fertility and

C Characterized by hypogonadotropic male external/internal genitalia, associated with
Because pituitary
the levels
hypogonadism and anosmia (loss of sense of tall stature, acne, and learning disabilities.
can't sense

of testosterone smell).

Caused by a deficiency in GnRH, leading to

decreased LH and FSH levels. Kallmann Syndrome Presence of ovaries with ambiguous external
/
genitalia.
-5 :
KAL-1
Primarily affects males, leading to delayed or gene
Mutation
absent puberty, small testes, and micropenis. Impaired Migration Exposure of XX individuals to excessive
Cryptorchidism
appear
normal .
also seen
,
but newborn females
of
to
GnRH neurons

Hypothalamus
Disorders of Sexual XX DSD
androgens, often due to congenital adrenal
hyperplasia (CAH) or gestational

Gonadal dysgenesis in XY individuals, leading

No Sertoli celle >
-

ducts
No MIH

develop
Development (DSD) hyperandrogenism.
&.. Mullerian

to female external genitalia, but with fibrous But No

functioning
ovaries to
Fetal vulnerability occurs between 7-12 weeks

Telegram Link
streak gonads. + No ovaries estrogen
produce
Types of DSD of gestation.
Swyer Syndrome

@medtalkss00
dlt non- Associated with the absence of puberty, lack of Presence of testes with ambiguous or female
functioning menstruation, and increased risk of gonadal external genitalia.
ovaries :
malignancy. Usually given estrogen supplements
No
Estrogen XY DSD
Caused by underexposure to androgens, due to
Autosomal recessive disorder leading to an conditions like gonadal dysgenesis, 5-α
blind
inability to convert testosterone to DHT. reductase deficiency, androgen insensitivity, or
Often connect to a

ending vagina testosterone synthesis defects.

Male internal genitalia develop, but external 5-α Reductase Deficiency
genitalia are predominantly female. XY DSD Specific Disorders
Affects 46, XY individuals:
↑ testosterone Often identified at puberty when BIL undescended testis Most common cause: 21-α hydroxylase
& I muscle
growth masculinization occurs. Male testosterone levels deficiency (90% of cases).
Absence of uterus

Congenital Adrenal Hyperplasia (CAH)

present Symptoms include hypoglycemia, salt loss,
Mutation in the androgen receptor of XY
individuals, leading to no response to
No internal
genitalia
sealoli all Leads to reduced cortisol and aldosterone hyperkalemia, ambiguous genitalia in XX
&It MIH from
androgens. production and increased androgen synthesis. individuals, and precocious puberty in XY
which inhibit Mullerian ducts
individuals.
Presents with female external genitalia and Complete Androgen Insensitivity Syndrome
Maternal androgen excess during pregnancy Mother hirsutism
abdominal testes, but no uterus or menstruation. (CAIS) develops
can cause virilization of XX fetuses.
form in utero dif SRY Gene
testosterone & DHT cannot L
ambiguous genitalia
& virilization
Breast development occurs at puberty due to
Both
Disorders of Androgen Excess Gestational Hyperandrogenism Secrete Testosterone

act
&: there is no internal & Causes include luteomas (rare gestational
the conversion of testosterone to estrogen, but
no pubic or armpit hair.
external
genitalia development tumors) or maternal use of androgenic drugs.

Deficiency in placental aromatase leads to

decreased conversion of testosterone to
Can present as separate ovaries and testes or estradiol, causing androgen excess in both
as ovotestes (both tissue types in one structure). mother and fetus.
Presence of both ovarian and testicular tissue in Placental Aromatase Deficiency
the same individual.
80% of cases occur in XX individuals. Results in virilization of the mother and
Ovotesticular DSD ambiguous genitalia in XX fetuses.
infertile
Mostly
·

Features include ambiguous genitalia, abnormal

breast development vagina, hypoplastic uterus, and undescended Dx-Gonadal Biopsy
·
At
Puberty -

testes.
menstruation occur
& may
 Meningitis and encephalitis can disrupt the BBB,
allowing pathogens and immune cells to enter
the brain.
Infections and Inflammation
Inflammation increases BBB permeability,
leading to potential damage from immune cell
infiltration.

Many brain tumors secrete factors that disrupt

the BBB, allowing angiogenesis (growth of new Brain Tumors
blood vessels) and tumor growth.

Disruption of the BBB is seen in conditions like The blood-brain barrier (BBB) is a selective
Alzheimer's disease, multiple sclerosis, and permeability barrier that protects the brain
Parkinson's disease. from harmful substances in the bloodstream
Neurodegenerative Diseases while allowing essential nutrients to pass
In Alzheimer's disease, the breakdown of the through.
Overview
BBB may contribute to the accumulation of
amyloid plaques. Clinical Implications of BBB It consists of tightly packed endothelial cells in
Dysfunction the capillaries of the brain, surrounded by
The BBB is a significant obstacle for delivering astrocyte end-feet and pericytes.
therapeutic drugs to the brain.

Using lipophilic drugs that can pass through Endothelial cells are connected by tight
Drug Delivery
passive diffusion. junctions, which limit the movement of
substances between cells.
Nanoparticles or liposomes to transport drugs Some strategies for overcoming this barrier
across the BBB. include: Astrocytes provide structural and functional
Key Features of the BBB support to the BBB by regulating the transport
Temporarily disrupting the BBB using focused of ions and maintaining the ionic environment.
ultrasound or osmotic agents.
Pericytes are embedded within the basement
Vasogenic/Cerebral Ischemic stroke can lead to the breakdown of
the BBB, contributing to further brain injury Stroke
membrane of the capillaries and contribute to
the integrity and function of the BBB.
Edemo
I of through edema and inflammatory responses.
swelling
brain tissue

Form the inner lining of blood vessels in the

Regions of the brain where the BBB is either brain.
absent or significantly reduced.
Have tight junctions that prevent the passive
These areas allow direct communication
between the blood and the brain to detect Circumventricular Organs (CVOs)
Blood-Brain Barrier Endothelial cells: diffusion of solutes between the blood and the
brain.
plasma composition or release hormones.
Vascular brain structures around ventricles (BBB)
Transport nutrients like glucose through
Area postrema (vomiting center) specific transport proteins.

= Subfornical organ (regulates fluid balance) Examples include: Extend their end-feet to surround the
endothelial cells.
Median eminence (involved in the release of
OULT
Components of the BBB
Allows
hypothalamic hormones) regulate hypothalames to
Regulate blood flow and maintain the
pituitary gland Astrocytes:
extracellular ion balance in the brain.
Posterior
Pituitary Oxytocin
-

,
ADH
Other Areas
(directly in
Pineal Gland Melatonin a

Provide metabolic support to neurons.

Allows small, lipophilic molecules to pass
through the BBB (e.g., oxygen, carbon dioxide, Passive Diffusion
Embedded in the basement membrane of brain
alcohol).
capillaries.
Pericytes:
Specific transport proteins allow the passage
of essential molecules like glucose and amino Contribute to the stability and maintenance of
acids. the BBB.
Facilitated Transport Transport Mechanisms
The glucose transporter (GLUT1) and amino
acid transporters are examples of facilitated Protects the brain from toxins, pathogens, and
transport mechanisms. fluctuating plasma concentrations of ions,
neurotransmitters, and hormones.
P-glycoprotein and other transporters actively
pump out harmful substances, including many Active Efflux Allows selective transport of nutrients (e.g.,
drugs, from the brain. Functions of the BBB glucose, amino acids) and essential ions.

Prevents entry of large or hydrophilic

molecules, as well as many drugs.
u

W
 Volume: 50-100 cc of air. Adverse Event: An incident resulting in harm to
the patient.
Sudden desaturation during thyroid, head/neck,
or CNS surgery. Near Miss: An incident that could have resulted
Clinical Presentation: Events in Patient Safety in harm but was prevented either by chance or
Often associated with sitting position. timely intervention.

Air Embolism No-Harm Event: An incident that reaches the

patient but results in no harm due to chance or
mitigating circumstances.

Air remains in the right side of the heart.

Management:
Air can be aspirated through a central line or
direct aspiration under image guidance.

Most common complication of cannula

insertion.
Durant position (left lateral legs up position):

Symptoms: Cord-like structure, pain, fever; can

persist for 3-4 months.

Treatment: Topical thrombophobe ointment.

Most common position for abdominal and
breast surgeries.

Superficial Thrombophlebitis:
IV Cannulas  Complications

Supine Position

Used for pelvic surgeries.

2.0 Patient Safety,
OT Zones, and
Feet raised, head lowered.
Surgical Positions

Trendelenburg Position

Used for laparoscopic cholecystectomy.

Head raised, feet lowered.

Written consent from the patient.

Confirm identity of the patient.

Sign In (Before Induction of Anaesthesia)
Confirm site marking.
Reverse Trendelenburg Position
Inquire about allergies.

Reconfirm identity of the patient.

Name of procedure.
Surgical Safety Checklist Time Out (Before Skin Incision) Surgeon:
Used for obstetric, gynecological, and Estimated blood loss.
urological procedures.
Anaesthetist: Antibiotic prophylaxis given.
Complication: Common peroneal nerve injury if
legs are unsupported. Nurse: Gauze and instrument count.
Sign Out (Before Patient Leaves Operating
Anaesthetist: Actual blood loss.
Room)

Lithotomy Position Surgeon: Specimen labeling.

Change rooms, transfer bay, pre/post-op

OT Positions Protective Zone:
rooms, ICU/PACU.
Thoracotomy.
Connects protective zone to aseptic zone,
Pyelolithotomy.
OT Zones Clean Zone: includes equipment store room and
Uses: maintenance workshop.
Nephrolithotomy.
Aseptic Zone: Operating Theater (OT).
Nephrectomy.
Disposal Zone: Waste disposal.
Complication: Brachial plexus injury if arms are
hyperextended.

Lateral or Kidney Position

Used for spinal surgery and pilonidal sinus

surgery.

Prone Position

Used for posterior cranial fossa surgeries.

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Bloodless field.
Advantages:
Good exposure.

Risk of air embolism if veins are nicked. Disadvantages:

Sitting/Fowler’s Position

Previously used for hemorrhoid and fissure

surgeries.

Rarely used now due to the risk of positional

asphyxia.
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Jack Knife Position

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Staining Techniques
Table 7. Gram Stain
Reagent Gram-Positive Gram-Negative

Crystal violet (a very intense purple, small dye Purple/Blue Purple/Blue

molecule)

Iodine (a large dye complex) Purple/Blue Purple/Blue

Acetone or Alcohol (a pale dye) Purple/Blue Colorless

Safranin (counterstain) Purple/Blue Red/Pink

● All cocci are gram-positive except Neisseria, Moraxella, and Veillonella.

● All spore formers are gram-positive.
● Background in stain modified for tissues will be pale red.

Table 8. Ziehl-Neelsen Acid Fast Stain (or Kinyoun)

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Table 8. Ziehl-Neelsen Acid Fast Stain (or Kinyoun)

Reagent Acid Fast Non-Acid Fast

Carbol Fuchsin with heat** Red (Hot Pink) Red (Hot Pink)

Acid Fast Bacili

Acid Alcohol Red Colorless

Methylene Blue*** Red Blue

Footnotes:

● Mycobacterium is acid fast. Nocardia is partially acid fast. All other bacteria are non-acid
fast.
● Three protozoan parasites (Cryptosporidium, Cystoisospora, and Cyclospora) have acid-fast
oocysts.
● **Without heat, the dye would not go in the mycobacterial cells.
● ***Sputa and human cells will be blue.

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Stages of Syphilis
Table 24. Stages of Syphilis
Stage Clinical Diagnosis

Primary (10 d to 3 mo Nontender chancre; clean, indurated Fluorescent microscopy of

post-exposure) edge; contagious; heals spontaneously lesion
3–6 weeks
50% of patients will be
negative by nonspecific
serology
=>

Secondary (1 to 3 mo Maculopapular (copper-colored) rash, Serology nonspecific and

later) diffuse, includes palms and soles, patchy specific; both positive
alopecia

Condylomata lata: flat, wartlike perianal

and mucous membrane lesions; highly
infectious

Latent None Positive serology

Tertiary (30% of Gummas (syphilitic granulomas), aortitis, Serology: specific tests

untreated, years later) CNS inflammation (tabes dorsalis) Nonspecific may be negative

Congenital (babies of IV Stillbirth, keratitis, 8th nerve damage, Serology: should revert to
drug-users) notched teeth; most born asymptomatic negative within 3 mo of birth
or with rhinitis → widespread if uninfected
desquamating maculopapular rash
PTO

mulberry molars

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40
 Weight loss in insulin deficiency (type 1
diabetes)

Obesity in type 2 diabetes

A severe deformity resulting from neuropathy Charcot neuroarthropathy: Dry mouth, reduced tissue turgor
12. Additional Signs of 1. General Observation Dehydration:
Yellowish plaques near the eyes, indicative of
Xanthelasma:
Complications Kussmaul breathing (in diabetic ketoacidosis)
dyslipidemia
A common infection in poorly controlled
Mucosal candidiasis:
diabetes

Eye movements, ptosis (drooping eyelid) Check for cranial nerve palsies:
11. Neurological Examination Measure blood pressure at every clinical visit
Particularly in the feet and lower limbs
Assess sensation and reflexes:
(sensorimotor neuropathy) 2. Blood Pressure
Look for signs of hypertension, a common
complication in diabetes

Thickening of subcutaneous fat due to

repeated injections
Inspect for lipohypertrophy: Acanthosis nigricans (neck, axillae): Darkened, velvety skin in insulin resistance
Impairs insulin absorption, leading to erratic
glucose control 10. Insulin Injection Sites Rash with scarred central yellow area on the
Necrobiosis lipoidica diabeticorum:
shins
Look for erythema, bruising, or infection
3. Skin Examination Diabetic bullae: Painless blisters on the skin

Granuloma annulare: Circular lesions often found on the skin

Seen in peripheral neuropathy Muscle wasting:
Vitiligo: Associated with autoimmune diabetes (type 1)
Loss of sensation in peripheral neuropathy Sensory abnormalities:

Indicative of poor circulation Hair loss: 9. Legs

Clinical Examination
Absent or diminished tendon reflexes in
of Diabetes Mellitus Visual acuity:
Check distance vision using a Snellen chart

Reflexes:
advanced neuropathy Check near vision using a reading chart

Look for a normal red reflex with an

4. Eyes Cataracts and lens opacity:
ophthalmoscope
Fatty liver infiltration, common in type 2
diabetes
Hepatomegaly: 8. Abdomen
Examine for signs of diabetic retinopathy
Fundoscopy:
Look for photocoagulation scars from previous
Check for ulcers, skin breaks, discoloration, laser treatments
callus formation

Look for fungal infections between the toes or Check carotid pulse
on the nails
Inspection: 5. Neck Examination Auscultate for carotid bruits
Clawing of toes or loss of the plantar arch,
indicating neuropathy Associated with autoimmune thyroid disease in
Inspect for thyroid enlargement:
type 1 diabetes
Severe deformities, which may indicate Charcot
neuroarthropathy

Dorsalis pedis and posterior tibial pulses "Prayer sign" shows an inability to fully extend
Limited joint mobility (cheiroarthropathy):
Palpate peripheral pulses: 7. Feet fingers
Absence indicates moderate risk of ulceration
6. Hands Dupuytren's contracture: Thickened skin and nodules over the palms
Use a 10-gram monofilament to check for
reduced sensation Carpal tunnel syndrome: Tingling and numbness in the hands
Sensation testing:
Loss of sensation in the feet increases the risk Muscle wasting or sensory changes: Indicative of peripheral neuropathy
of foot ulcers

Ankle reflexes may be lost in severe neuropathy Reflexes:

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