Pathophysiology

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Pathophysiology sample values
BMP/ELECTROLYTES:
Na+
= 140 		Cl− = 100 BUN = 20 /
Glu = 150
\
K+ = 4 CO2 = 22 PCr = 1.0
ARTERIAL BLOOD GAS
:
HCO3− = 24 paCO2 = 40 paO2 = 95 pH = 7.40
ALVEOLAR GAS:
pACO2 = 36 pAO2 = 105 A-a g = 10
OTHER:
Ca = 9.5 Mg2+ = 2.0 PO4 = 1
CK = 55 BE = −0.36 AG = 16
SERUM OSMOLARITY/RENAL
:
PMO = 300 PCO = 295
POG
= 5
BUN:Cr
= 20
URINALYSIS:
UNa+ = 80 UCl− = 100 UAG = 5
FENa
= 0.95
UK+ = 25 USG = 1.01 UCr = 60 UO = 800
PROTEIN/GI/LIVER FUNCTION TESTS:
LDH = 100 TP = 7.6 AST = 25 TBIL = 0.7
ALP = 71 Alb = 4.0 ALT = 40 BC = 0.5
AST/ALT = 0.6 BU = 0.2
AF alb
= 3.0 		SAAG = 1.0
SOG
= 60
CSF:
CSF alb = 30 CSF glu = 60 CSF/S alb = 7.5 CSF/S glu = 0.6

Pathophysiology (or physiopathology) is a branch of study, at the intersection of pathology and physiology, concerning disordered physiological processes that cause, result from, or are otherwise associated with a disease or injury. Pathology is the medical discipline that describes conditions typically observed during a disease state, whereas physiology is the biological discipline that describes processes or mechanisms operating within an organism. Pathology describes the abnormal or undesired condition, whereas pathophysiology seeks to explain the functional changes that are occurring within an individual due to a disease or pathologic state.[1]

Etymology

The term pathophysiology comes from the Ancient Greek πάθος (pathos) and φυσιολογία (phisiologia).

History

Nineteenth century

Reductionism

In Germany in the 1830s,

Julius Cohnheim pioneered experimental pathology in medical schools' scientific laboratories.[citation needed
]

Germ theory

By 1863, motivated by

Jakob Henle's postulates, and confirmed Davaine's conclusion, a major feat for experimental pathology. Pasteur and colleagues followed up with ecological
investigations confirming its role in the natural environment via spores in soil.

Also, as to

aniline dyes to identify particular microorganisms for each.[3] Germ theory of disease crystallized the concept of cause—presumably identifiable by scientific investigation.[4]

Scientific medicine

The American physician

Howard Kelly, and William Halsted— opened at last in 1893 as America's first medical school devoted to teaching German scientific medicine, so called.[5]

Twentieth century

Biomedicine

The first biomedical institutes,

The Rockefeller Institute for Medical Research, was founded in 1901 with Welch, nicknamed "dean of American medicine", as its scientific director, who appointed his former Hopkins student Simon Flexner as director of pathology and bacteriology laboratories. By way of World War I and World War II, Rockefeller Institute became the globe's leader in biomedical research.[citation needed
]

Molecular paradigm

The

Oswald Avery, America's leading pneumococcal expert, was so troubled by the report that they refused to attempt repetition.[9]

When Avery was away on summer vacation, Martin Dawson, British-Canadian, convinced that anything from England must be correct, repeated Griffith's results, then achieved transformation in vitro, too, opening it to precise investigation.[9] Having returned, Avery kept a photo of Griffith on his desk while his researchers followed the trail. In 1944, Avery, Colin MacLeod, and Maclyn McCarty reported the transformation factor as DNA, widely doubted amid estimations that something must act with it.[10] At the time of Griffith's report, it was unrecognized that bacteria even had genes.[11]

The first genetics,

double helix— and conjectured it to spell a code. In the early 1960s, Crick helped crack a genetic code in DNA, thus establishing molecular genetics
.

In the late 1930s,

light microscopy.[12] Around 1940, largely via cancer research at Rockefeller Institute, cell biology emerged as a new discipline filling the vast gap between cytology and biochemistry by applying new technology —ultracentrifuge and electron microscope— to identify and deconstruct cell structures, functions, and mechanisms.[12] The two new sciences interlaced, cell and molecular biology.[12]

Mindful of

Phage Group —hosting Watson— discovering details of cell physiology by tracking changes to bacteria upon infection with their viruses, the process transduction. Lederberg led the opening of a genetics department at Stanford University's medical school, and facilitated greater communication between biologists and medical departments.[14]

Disease mechanisms

In the 1950s, researches on

Memorial Sloan–Kettering Cancer Center, Thomas collaborated with Lederberg, soon to become president of Rockefeller University, to redirect the funding focus of the US National Institutes of Health toward basic research into the mechanisms operating during disease processes, which at the time medical scientists were all but wholly ignorant of, as biologists had scarcely taken interest in disease mechanisms.[16] Thomas became for American basic researchers a patron saint.[17]

Examples

Parkinson's disease

The

mitochondrial function, neuroinflammation, and blood–brain barrier (BBB) breakdown resulting in vascular leakiness.[18]

Heart failure

The pathophysiology of heart failure is a reduction in the efficiency of the heart muscle, through damage or overloading. As such, it can be caused by a wide number of conditions, including myocardial infarction (in which the heart muscle is starved of oxygen and dies), hypertension (which increases the force of contraction needed to pump blood) and amyloidosis (in which misfolded proteins are deposited in the heart muscle, causing it to stiffen). Over time these increases in workload will produce changes to the heart itself.

Multiple sclerosis

The

inflammatory demyelinating disease of the CNS in which activated immune cells invade the central nervous system and cause inflammation, neurodegeneration and tissue damage. The underlying condition that produces this behaviour is currently unknown. Current research in neuropathology, neuroimmunology, neurobiology, and neuroimaging, together with clinical neurology provide support for the notion that MS is not a single disease but rather a spectrum[19]

Hypertension

The

idiopathic) or secondary. About 90–95% of hypertension is essential hypertension.[20][21][22][23]

HIV/AIDS

The

opportunistic infections and certain forms of cancer
.

Spider bites

The pathophysiology of spider bites is due to the effect of its venom. A spider envenomation occurs whenever a spider injects venom into the skin. Not all spider bites inject venom – a dry bite, and the amount of venom injected can vary based on the type of spider and the circumstances of the encounter. The mechanical injury from a spider bite is not a serious concern for humans.

Obesity

The pathophysiology of obesity involves many possible pathophysiological mechanisms involved in its development and maintenance.[25] This field of research had been almost unapproached until the leptin gene was discovered in 1994 by J. M. Friedman's laboratory.[26] These investigators postulated that leptin was a satiety factor. In the ob/ob mouse, mutations in the leptin gene resulted in the obese phenotype opening the possibility of leptin therapy for human obesity. However, soon thereafter J. F. Caro's laboratory could not detect any mutations in the leptin gene in humans with obesity. On the contrary Leptin expression was increased proposing the possibility of Leptin-resistance in human obesity.[27]

See also

References

  1. ^ "Pathophysiology – Medical dictionary". TheFreeDictionary.com. Farlex, Inc.
  2. PMID 5325873
    .
  3. ^ a b c Bulloch, William, The History of Bacteriology (Oxford: Oxford University Press, 1938 & 1960 / New York: Dover Publications, 1979), p 143–144, 147-148
  4. PMID 6997653
    .
  5. ^
    PMID 21738298
    .
  6. PMID 11049162
    .
  7. ^ "In the bacteriology of the 1920s, the conversion of the R to the S form could be regarded as an adaptation to the environment. However, the transformation of Type I to Type II was the equivalent of the transformation of one species into another, a phenomenon never before observed. Avery was initially skeptical of Griffith's findings and for some time refused to accept the validity of his claims, believing that they were the result of inadequate experimental controls. Avery's research on therapeutic sera led him to conclude that pneumococcal types were fixed and that specific therapeutic agents could thus be developed to combat the various types. A transformation from type to type in vivo presented a disturbing clinical picture, as well as a challenge to the theoretical formulations of contemporary bacteriology" [Oswald T Avery Collection, "Shifting focus: Early work on bacterial transformation, 1928-1940", Profiles in Science, US National Library of Medicine, Web: 24 Jan 2013].
  8. ^ Dubos, René J, Oswald T Avery: His Life and Scientific Achievements (New York: Rockefeller University Press, 1976), pp 133, 135-136
  9. ^ a b Dubos, René, "Memories of working in Oswald Avery's laboratory", Symposium Celebrating the Thirty-Fifth Anniversary of the Publication of "Studies on the chemical nature of the substance inducing transformation of pneumococcal types", 2 Feb 1979
  10. ^ Lederberg J (1956). "Notes on the biological interpretation of Fred Griffith's finding". American Scientist. 44 (3): 268–269.
  11. PMID 12486033
    .
  12. ^ a b c d e Bechtel, William, Discovering Cell Mechanisms: The Creation of Modern Cell Biology (New York: Cambridge University Press, 2005)
  13. ^ Kay, Lily, Molecular Vision of Life: Caltech, the Rockefeller Foundation, and the Rise of the New Biology (New York: Oxford University Press, 1993)
  14. ^
    ISBN 978-0-309-13121-6
    .
  15. PMC 2118519
    .
  16. ^ Letter: Lewis Thomas (MSKCC) to Joshua Lederberg (Stanford Univ), 7 Aug 1978, p 1
  17. PMID 16648878
    .
  18. PMID 19913097
    .
  19. S2CID 20562972
    .
  20. PMID 10645931
    . Retrieved 2009-06-05.
  21. S2CID 32785528
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  22. ISBN 0-7216-0240-1
    .
  23. ^ "Hypertension: eMedicine Nephrology". Retrieved 2009-06-05.
  24. PMID 26962940
    .
  25. PMID 14744442
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  26. S2CID 4359725
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  27. PMID 7769141
    .
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