Isi Laporan Tutorial Skenario B Blok 15

CHAPTER I
INTRODUCTION
1.1 Background
Urinary and Male Reproduction System is the 15th block on semester 5 of
Kurikulum Berbasis Kompetensi (KBK) system in Medical Faculty of
Muhammadiyah Palembang University. One of the strategy from these
curriculum is Problem Based Learning (PBL). Case tutorial is one of the
implementation of this PBL methode. In this section, Students are divided
into small groups and every groups will be guided by a mentor or a lecturer as
a facilitator who will guide the students to solve the case.
Tutorial process is a part of student’s evaluation exactly as a formative
evaluation. These evaluation helps the students to reach the aim of study.
Tutorial process is also requirment for students to join the block’s exam
called OSOCA (Objective Structure Oral Case Analysis) which is included in
summative evaluation. The aim of summative evaluation is assesing the
student’s achievement in order to determine the competencies that have been
achieved. Summative assessment is done by referring to the learning
taxonomy proposed by Bloom that consist of cognitive, psychomotor, and
affective assessment.
1.2 Purpose and Objectives

The purpose and objectives of this case study tutorial, namely:
1. As a report task group tutorial that is part of KBK learning system at the
Faculty of Medicine, Muhammadiyah University of Palembang.
2. Can solve the case given in the scenario with the method of analysis and
learning group discussion.
3. Achieving the objectives of the tutorial learning method.
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CHAPTER II
DISCUSSION
2.1 Tutorial’s Data

Tutor : dr. H. Achmad Azhari, DAHK.
Moderator : M. Avif Ababil
Secretary : Bella Juni Safira
Notulis : Delis Qurrota A’yun
Date and Time :
1. Tuesday, November 7th 2017
Time : 08.00 – 10.30 a.m
2. Thursday, November 9th 2017
Time : 08.00 – 10.30 a.m
Rules :
1. Everyone in the group should express their opinion
2. Gadget should be nonactive or in silent mode.
3. Ask for permission if want to go outside.
4. Eating and drinking are not allowed in the room.
2.2 Case Scenario

"My eyes are swollen"
Ibnu, boy, 7 years old, brought to Pediactric Clinic RSMP with chief
complaints is swollen of a whole body. Swollen appeared since 5 days ago.
Swollen first appears around the eyelids and testicles, especially after
awakening, then comes up in face, both the legs and back of foot. Ibnu also
complained of headaches, but no blurry vision and no dyspnue. Urine volume
about one glass per days and red like water of meat wash. Two weeks before
the swollen, Ibnu suffered scabs in the area of legs. Ibnu didn’t seek
treatment and his scabs dry themselves. These symptoms are the first
experienced. No family suffers the same.
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Physical Examination :
General Condition
Compos mentis, moderate illnes , body weight 28 kg, height 113 cm.
Vital Signs
BP 140/90 mmHg, pulse 96 x/min, RR 28 x/min, body temperature 36.8OC.
Specific Circumstances
Head : palpebrals edema, anemic conjunctivas
no hyperemic pharynx, tonsils are normal
Neck : no lymp gland enlargement
Chest : pulmo: sound vesicular ,no rhales, no wheezing
Heart: heart sound I / II normal, no murmur
Abdomen : buldging, tender, with shifting dullness,
liver and lien are not palpable, normal bowel sound
Extremities: pitting edema, dorsum pedis edema
2.3 Clarification of Terms

1. Swollen is transient abnormal enlargement of a body part or area not due
to cell proliferation.
2. Headaches is a pain in head. Pain is a feeling of distress, suffering, or
agony, caused by stimulation of specialized nerve endings.
3. Palpebra edema is an abnormal accumulation of fluid in intercelullar
spaces of the body especially in the eyelids.
4. Scabs is the crust of a superficial sore
5. Shifting dullness is a sign on physical examination or ascites (fluid in the
peritoneal cavity) diminished resonance on percussion also a peculiar
percussion sound which lacks the normal resonance.
6. Pitting edema is an abnormal accumulation of fluid in intercelullar spaces
of the body that in which pressure leaves a persistent depression in the
tissues.
7. Anemic conjunctivas is a reduction below normal of the number of
erythrocytes, quantity of hemoglobin, or the volume of packed red cells in
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the blood in the delicate membrane lining the eyelids and covering the
eyeballs.
8. Red like water of meat wash urine (Haematuria) is a erythrocyte in the
urine.
9. One glass per days urine volume (Oliguria) is diminished urine production
and excretion in relation to fluid intake.
10. Testicles is the male gonad; either the paired egg-shaped gland normally
situated in the scrotum, in which the spermatozoa develop. Specialized
interstitial cells (Leydig cells) secrete testosterone.
2.4 Problem Identification

1. Ibnu, a boy, 7 year old, brought his parents to Pediactric Clinic RSMP
with chief complaints of swollen whole body. Swollen appeared since 5
days ago. Swollen first appears around the eyelids and testicles, especially
after awakening then in face, both the legs and back of foot.
2. Ibnu also complained of headaches, but no blurry vision and no dyspnue.
3. Urine volume about one glass per days and red like water meat wash.
4. Two weeks before appears of swollen, Ibnu suffered from scabs in the area
of legs. Ibnu didn’t seek treatment and his scabs dry themselves. The
symptoms of this disease first experienced. No family suffers from this
disease.
5. Physical Examination :
Vital Signs : BP 140/90 mmHg, weight 28 kg, height 113 cm.
Specific Circumstances:
Head : edema palpebra (+)/(+), pale conjunctiva (+)
Chest : Lung : vesicular (+) normal, ronki (-), wheeze (-)
Heart : heart sound I / II normal, noisy (-)
Abdomen : convex, limp, shifting dullness (+), tenderness (-),
Extremities : pitting (+)/(+) edema, edema dorsum pedis (+)/(+)
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2.5 Problem analysis
1. Ibnu, a boy, 7 year old, brought his parents to Pediactric Clinic RSMP
with chief complaints of swollen whole body. Swollen appeared since 5
days ago. Swollen first appears around the eyelids and testicles,
especially after awakening then in face, both the legs and back of foot.
a. What are organs involved in this case? (kidney)
Answer:
The organs that involved in this case are kidneys.
Synthesis:
The paired kidneys are reddish, kidney-bean-shaped organs located
just above the waist between the peritoneum and the posterior wall of
the abdomen. Because their position is posterior to the peritoneum of
the abdominal cavity, they are said to be retroperitoneal organs. The
kidneys are located between the levels of the last thoracic and third
lumbar vertebrae, a position where they are partially protected by the
eleventh and twelfth pairs of ribs. The right kidney is slighlty lower
than the left because the liver occupies considerable space on the right
side superior to the kidney (Tortora&Derrickson, 2007: 994).
Picture 1.1 Right Kidney, coronal section
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Source: Mescher, 2013 (Junqueira’s Basic Histology)
b. How is the anatomy, physiology and histology of organs involved
in this case?
Answer:
The paired kidneys are reddish, kidney-bean-shaped organs located
just above the waist between the peritoneum and the posterior wall of
the abdomen. Because their position is posterior to the peritoneum of
the abdominal cavity, they are said to be retroperitoneal organs. The
kidneys are located between the levels of the last thoracic and third
lumbar vertebrae, a position where they are partially protected by the
eleventh and twelfth pairs of ribs. The right kidney is slighlty lower
than the left because the liver occupies considerable space on the right
side superior to the kidney (Tortora&Derrickson, 2007: 994).
Picture 1.2 Kidneys

Source: Tortora&Derrickson, 2007
External anatomy of the Kidneys
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A typical adult kidney is 10-12 cm (4-5 in.) long, 5-7 cm (2-3 in.)
wide, and 3 cm (1 in.) thick—about the size of a bar of bath soap—
and has a mass of 135-150 g (4.5-5 oz). The concave medial border of
each kidney faces the vertebral column. Near the center of the concave
border is a deep vertical fissure called the renal hilum, through which
the ureter emerges from the kidney along with blood vessels,
lymphatic vessels, and nerves (Tortora&Derrickson, 2007: 994).
Picture 1.3 Frontal Section of Right Kidney

Source: Tortora&Derrickson, 2007
Three layers of tissue surround each kidney. The deep layer, the
renal capsule, is a smooth, transparent sheet of dense irregular
connective tissue that is continuous with the outer coat of the ureter. It
serves as a barrier against trauma and helps maintain the shape of the
kidney. The middle layer, the adipose capsule, is a mass of fatty tissue
surrounding the renal capsule. It also protects the kidney from trauma
and holds it firmly in place within the abdominal cavity. The
superficial layer, the renal fascia, is another thin layer of dense
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irregular connective tissue that anchors the kidney to the surrounding
structures and to the abdominal wall. On the anterior surface of the
kidneys, the renal fascia is deep to the peritoneum
(Tortora&Derrickson, 2007: 994).
Internal anatomy of the kidneys

A frontal section through the kidney reveals two distinct regions: a
superficial, smooth-textured reddish area called the renal cortex and a
deep, reddish-brown inner region called the renal medulla. The renal
medulla consists of several cone-shaped renal pyramids. The base
(wider end) of each pyramid faces the renal cortex, and its apex
(narrower end), called a renal papilla, points toward the renal hilum.
Picture 1.4 Nephrons

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The renal cortex is the smooth-textured area extending from the
renal capsule to the bases of the renal pyramids and into the spaces
between them. It is divided into an outer cortical zone and an inner
juxtamedullary zone. Those portions of the renal cortex that extend
between renal pyramids are called renal column. A renal lobe consists
of a renal pyramid, its overlaying area of the renal cortex, and one-half
of each adjacent renal column (Tortora&Derrickson, 2007: 997).
Together, the renal cortex and renal pyramids of the renal medulla
constitute the parenchyma (functional portion) of the kidney. Within
the parenchyma are the functional units of the kidney—about 1
million microscopic structures called nephrons. Urin formed by the
nephrons drains into large papillary ducts, which extend through the
renal papillae of the pyramids. The papillary ducts drain into cuplike
structures called minor and major calyces. Each kidney has 8 to 18
minor calyces and 2 to 3 major calyces. A minor calyx receives urine
from the papillary ducts of one renal papilla and delivers it to a major
calyx. From the major calyces, urine drains into a single large cavity
called the renal pelvis and then out through the ureter to the urinary
bladder (Tortora&Derrickson, 2007: 997).
The hilum expands into a cavity within the kidney called the renal
sinus, which contains part of the renal pelvis, the calyces, and
branches of the renal blood vessels and nerves. Adipose tissue helps
stabilize the position of thse structures in the renal sinus
Blood and nerve supply of the kidney

Because the kidneys remove wastes from the blood and regulate its
volume and ionic composition, it is not surprisingly that they are
abundantly supplied with blood vessels. Although the kidneys
constitute less than 0.5% of total body mass, they receive 20-25% of
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the resting cardiac output via the right and left renal arteries. In adults,
renal blood flow, the blood flow through both kidneys, is about 1200
mL per minute (Tortora&Derrickson, 2007: 997).
Picture 1.5 Blood Supply of Kidneys
Within the kidney, the renal artery divides into several segmental
arteries, which supply different segments (areas) of the kidney. Each
segmental artery gives off several branches that enter the parenchyma
and pass through the renal columns between the renal pyramids as the
interlobar arteries. At the bases of the renal pyramids, the interlobar
arteries arch between the renal medulla and cortex; here they are
known as the arcuate arteries. Divisions of the arcuate arteries produce
a series of interlobular arteries. These arteries are so named because
they pass between renal lobules. Interlobular arteries enter the renal
cprtex and give off branches called afferent arterioles
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Each nephron receives one afferent arteriole, which divides into a
tangled, ball-shaped capillary network called the glomerulus. The
glomerular capillaries the reunite to form an effernt arteriole that
carries blood out of the glomerulus. Glomerular capillaries are unique
among capillaries in the body because they are positioned between
two arterioles, rather than between an arteriole and a venule. Because
they are capillary networks and they also play an important role in the
urine formation, the glomeruli are considered part of both the
cardiovascular and the urinary systems (Tortora&Derrickson, 2007:
997).
The efferent arterioles divide to form the peritubular capillaries,
which surround tubular parts of the nephron in the renal cortex.
Extending from some efferent arterioles are long loop-shaped
capillaries called vasa recta that supply tubular portions of the nephron
in the renal medulla (Tortora&Derrickson, 2007: 997).
The peritubular capillaries eventually reunite to form peritubular
venules and then interlobular veins, which also receive blood from the
vasa recta. Then the blood drains through the arcuate veins to the
interlobar veins running between the renal pyramids. Blood leaves the
kidney through a single renal vein that exists at the renal hilum and
carries venous blood to the inferior vena cava (Tortora&Derrickson,
2007: 997).
Most renal nerves originates in the celiac ganglion and pass
through the renal plexus into the kidneys along with the renal arteries.
Renal nerves are part of the symphatetic divisions of the autonomic
nervous system. Most are vasomotor nerves that regulate the floq of
blood through the kidney by causing vasodilatation or
vasoconstriction of renal arterioles (Tortora&Derrickson, 2007: 997).
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Histology and physiology of the nephron and Collecting Duct
Renal Function: Filtration, Secretion, & Reabsorption
All the major functions of the kidneys—the removal of metabolic
wastes and excess water and electrolytes from blood—are performed
by various specialized epithelial cells of the nephrons and collecting
systems. Renal function involves specific activities:
Filtration, by which water and solutes in the blood leave the vascular
space and enter the lumen of the nephron;
Tubular secretion, by which substances move from epithelial cells of
the tubules into the lumens, usually after uptake from the surrounding
interstitium and capillaries; and
Tubular reabsorption, by which substances move from the tubular
lumen across the epithelium into the interstitium and surrounding
capillaries. Along the length of the nephron tubule and collecting
system, the filtrate receives various secreted molecules while others
are reabsorbed and then enters the minor calyces as urine and
undergoes excretion. The number of nephrons decreases slightly in
older adults, a process accelerated by high blood pressure. If a kidney
is donated for transplant (unilateral nephrectomy), the remaining
kidney undergoes compensatory growth, with cellular hypertrophy in
the proximal parts of the nephron tubules and an increase in the rate of
filtration, which allow normal renal function to continue.
Renal Corpuscles & Blood Filtration

At the beginning of each nephron is a renal corpuscle, about 200
μm in diameter and containing a tuft of glomerular capillaries,
surrounded by a double-walled epithelial capsule called the
glomerular (Bowman) capsule. The internal or visceral layer of this
capsule closely envelops the glomerular capillaries, which are finely
fenestrated. The outer parietal layer forms the surface of the capsule.
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Between the two capsular layers is the capsular (or urinary) space,
which receives the fluid filtered through the capillary wall and visceral
layer. Each renal corpuscle has a vascular pole, where the afferent
arteriole enters and the efferent arteriole leaves, and a tubular pole,
where the proximal convoluted tubule (PCT) begins (Mescher, 2013).
Picture 1.6 Renal Corpuscle

The outer parietal layer of a glomerular capsule consists of a simple

squamous epithelium supported externally by a basal lamina. At the
tubular pole, this epithelium changes to the simple cuboidal
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epithelium that continues and forms the proximal tubule (Mesher,
2013).
The visceral layer of a renal corpuscle consists of unusual stellate
epithelial cells called podocytes, which together with the capillary
endothelial cells compose the apparatus for renal filtration. From the
cell body of each podocyte several primary processes extend and
curve around a length of glomerular capillary. Each primary process
gives rise to many parallel, interdigitating secondary processes or
pedicels (L. pedicellus, little foot;). The pedicels cover much of the
capillary surface, in direct contact with the basal lamina (Mescher,
2013).
Between the interdigitating pedicels are elongated spaces, or
filtration slit pores, 25 to 30 nm wide. Spanning adjacent pedicels and
bridging the slit pores are zipper-like slit diaphragms. Slit
diaphragms are modified and specialized occluding or tight junctions
composed of nephrins, other proteins, glycoproteins, and
proteoglycans important for renal function. Projecting from the cell
membrane on each side of the filtration slit, these polyanionic
glycoproteins and proteoglycans interact to form a series of openings
within the slit diaphragm, with a surface that is negatively charged
(Mescher, 2013).
Between the highly fenestrated endothelial cells of the capillaries
and the covering podocytes is the thick (300-360 nm) glomerular
basement membrane (GBM). This membrane is the most substantial
part of the filtration barrier that separates the blood from the capsular
space and forms by fusion of the capillary- and podocyte-produced
basal laminae. Laminin and fibronectin in this fused basement
membrane bind integrins of both the podocyte and endothelial cell
membranes, and the meshwork of cross-linked type IV collagen and
large proteoglycans restricts passage of proteins larger than about 70
kDa. Smaller proteins that are filtered from plasma are degraded, and
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the amino acids reabsorbed in the proximal tubule. Polyanionic GAGs
in the glomerular membrane are abundant and their negative charges,
like those of the slit diaphragms, tend to restrict filtration of organic
anions (Mescher, 2013).
Filtration, therefore, occurs through a structure with three parts
according to Mescher (2013):
1. The fenestrations of the capillary endothelium, which blocks blood
cells and platelets;
2. The thick, combined basal laminae, or GBM, which restricts large
proteins and some organic anions; and
3. The filtration slit diaphragms between pedicels, which restrict some
small proteins and organic anions.
Normally about 20% of the blood plasma entering a glomerulus is
filtered into the capsular space. The initial glomerular filtrate has a
chemical composition similar to that of plasma except that it contains
very little protein. The glomerular filter blocks filtration of most
plasma proteins, but smaller proteins, including most polypeptide
hormones, are removed into the filtrate (Mescher, 2013).
Capillaries of each glomerulus have a total length of approximately
1 cm and are uniquely situated between two arterioles—afferent and
efferent—the muscle of which allows increased hydrostatic pressure
in these vessels, favoring movement of plasma across the glomerular
filter. The glomerular filtration rate (GFR) is constantly regulated by
neural and hormonal inputs affecting the degree of constriction in each
of these arterioles. The total glomerular filtration area of an adult has
been estimated at 500 cm2 and the average GFR at 125 mL/min or
180 L/d. Because the total amount of circulating plasma averages 3 L,
it follows that the kidneys typically filter the entire blood volume 60
times every day (Mescher, 2013).
In addition to capillary endothelial cells and podocytes, renal
corpuscles also contain mesangial cells (Gr. mesos, in the midst +
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angion, vessel), most of which resemble vascular pericytes in having
contractile properties and producing components of an external
lamina. Mesangial cells are difficult to distinguish in routine sections
from podocytes, but often stain more darkly. They and their
surrounding matrix comprise the mesangium, which fills interstices
between capillaries that lack podocytes. Functions of the mesangium
include the following according to Mescher (2013):
1. Physical support of capillaries within the glomerulus;
2. Adjusted contractions in response to blood pressure changes,
which help maintain an optimal filtration rate;
3. Phagocytosis of protein aggregates adhering to the glomerular
filter, including antibody-antigen complexes abundant in many
pathological conditions; and
4. Secretion of several cytokines, prostaglandins, and other factors
important for immune defense and repair in the glomerulus.
Proximal Convoluted Tubule

Cells in many parts of the nephron tubule and collecting system
reabsorb water and electrolytes, but other activities are restricted
mainly to specific tubular regions. At the tubular pole of the renal
corpuscle, the simple squamous epithelium of the capsule’s parietal
layer is continuous with the simple cuboidal epithelium of the
proximal convoluted tubule (PCT). These long, tortuous tubules fill
most of the cortex. PCT cells are specialized for both reabsorption and
secretion. Over half of the water and electrolytes, and all of the
organic nutrients (glucose, amino acids, vitamins, etc), filtered from
plasma in the renal corpuscle are normally reabsorbed in the PCT.
These molecules are transferred directly across the tubular wall for
immediate uptake again into the plasma of the peritubular capillaries
(Mescher, 2013).
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Transcellular reabsorption involves both active and passive

mechanisms, with the cells having a large variety of transmembrane
ion pumps, ion channels, transporters, enzymes, and carrier proteins.
Water and certain solutes can also move passively between the cells
(paracellular transport) along osmotic gradients through leaky apical
tight junctions (Mescher, 2013).
Small proteins in the filtrate are either reabsorbed by receptor-
mediated endocytosis and degraded in the cuboidal cells, or degraded
by peptidases on the luminal surface. In both cases the amino acids are
released at the basolateral cell surfaces for uptake by capillaries.
Conversely, organic anions and cations not filtered in the renal
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corpuscle (because of the polyanions in the filter or binding to plasma
proteins) may be released in the peritubular capillaries, taken up by
the cells of the proximal tubules and undergo secretion into the
filtrate (Mescher, 2013).
Organic anion and cation transporters allow the kidneys to dispose
of such substances at a higher rate than by glomerular filtration alone.
Because these molecules include important substances (such as bile
salts, creatinine, etc) and many antibiotics and other drugs, this
process of tubular secretion is of great pharmacologic importance as a
key mechanism of drug clearance (Mescher, 2013).

The cells of the proximal tubules have central nuclei and very
acidophilic cytoplasm because of the abundant mitochondria. The cell
apex has very many long microvilli that form a prominent brush
border in the lumen that facilitates reabsorption. Because the cells are
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large, each transverse section of a PCT typically contains only three to
five nuclei. In routine histologic preparations, the long brush border
may be disorganized and give the lumens a fuzz-filled appearance.
Peritubular capillaries are abundant in the sparse surrounding
connective tissue interstitium, which fills only about 10% of the
cortex (Mescher, 2013).
Ultrastructurally the apical cytoplasm of these cells has numerous
pits and vesicles near the bases of the microvilli, indicating active
endocytosis and pinocytosis. These vesicles contain the small,
reabsorbed proteins that will be degraded in lysosomes, with the
amino acids released to the circulation. Proximal tubular cells also
have many long basal membrane invaginations and lateral
interdigitations with neighboring cells. Both the brush border and the
basolateral folds contain the many types of transmembrane proteins
that mediate tubular reabsorption and secretion. Long mitochondria
concentrated along the basal invaginations supply ATP locally for the
membrane proteins involved in active transport. Because of the
extensive interdigitations of the lateral membranes, discrete limits
between cells of the proximal tubule are difficult to see with the light
microscope (Mescher, 2013).
Besides their major roles in reabsorption and secretion, cells of the
proximal tubule also perform hydroxylation of vitamin D and release
to the capillaries. Moreover, fibroblastic interstitial cells in cortical
areas near the proximal tubules produce erythropoietin, the growth
factor secreted in response to a prolonged decrease in local oxygen
concentration (Mescher, 2013).
Loop of Henle
The PCT continues with the much shorter proximal straight tubule
that enters the medulla and continues the nephron’s loop of Henle.
This is a U-shaped structure with a thin descending limb and a thin
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ascending limb, both composed of simple squamous epithelia. The
straight part of the proximal tubule has an outer diameter of about 60
μm, but it narrows abruptly to about 30 μm in the thin limbs of the
loop. The wall of the thin segments consists only of squamous cells
with few organelles (indicating a primarily passive role in transport)
and the lumen is prominent. The thin ascending limb of the loop
becomes the thick ascending limb (TAL), with simple cuboidal
epithelium and many mitochondria again, in the outer medulla and
extends as far as the macula densa near the nephron’s glomerulus
(Mescher, 2013).
Picture 1.9 Histology of Nephrons

The loops of Henle and surrounding interstitial connective tissue

are involved in further adjusting the salt content of the filtrate.
Cuboidal cells of the loops’ TALs actively transport sodium and
chloride ions out of the tubule against a concentration gradient into the
hyaluronate-rich interstitium, making that compartment hyperosmotic.
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This causes water to be withdrawn passively from the thin descending
part of the loop, thus concentrating the filtrate. The thin ascending
limbs reabsorb sodium chloride (NaCl) but are impermeable to water.
The countercurrent flow of the filtrate (descending, then immediately
ascending) in the two parallel thin limbs establishes a gradient of
osmolarity in the interstitium of the medullary pyramids, an effect that
is “multiplied” at deeper levels in the medulla (Mescher, 2013).
Countercurrent blood flow in the descending and ascending loops
of the vasa recta helps maintain the hyperosmotic interstitium. The
interstitial osmolarity at the pyramid tips is about four times that of the
blood. The countercurrent multiplier system established by the
nephron loop and vasa recta is an important aspect of renal physiology
in humans (Mescher, 2013).
Distal Convoluted Tubule & Juxtaglomerular Apparatus

The ascending limb of the nephron is straight as it enters the cortex
and forms the macula densa, and then becomes tortuous as the distal
convoluted tubule (DCT). Much less tubular reabsorption occurs
here than in the proximal tubule. The simple cuboidal cells of the
distal tubules differ from those of the proximal tubules in being
smaller and having no brush border and more empty lumens. Because
distal tubule cells are flatter and smaller than those of the proximal
tubule, more nuclei are typically seen in sections of distal tubules than
in those of proximal tubules. Cells of the DCT also have fewer
mitochondria than cells of proximal tubules, making them less
acidophilic. The rate of Na+ absorption here is regulated by
aldosterone from the adrenal glands (Mescher, 2013).
Where the initial, straight part of the distal tubule contacts the
arterioles at the vascular pole of the renal corpuscle of its parent
nephron, its cells become more columnar and closely packed, forming
the macula densa (L. thicker spot). This is part of a specialized
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sensory structure, the juxtaglomerular apparatus (JGA) that utilizes
feedback mechanisms to regulate glomerular blood flow and keep the
rate of glomerular filtration relatively constant. Cells of the macula
densa typically have apical nuclei, basal Golgi complexes, and a more
elaborate and varied system of ion channels and transporters. Adjacent
to the macula densa, the tunica media of the afferent arteriole is also
modified (Mescher, 2013).
The smooth muscle cells are modified as juxtaglomerular
granular (JG) cells, with a secretory phenotype including more
rounded nuclei, rough ER, Golgi complexes, and zymogen granules
with renin. Also at the vascular pole are lacis cells (Fr. lacis,
lacework), which are extraglomerular mesangial cells that have many
of the same supportive, contractile and defensive functions as these
cells inside the glomerulus (Mescher, 2013).

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Basic functions of the JGA in the autoregulation of the GFR and in
controlling blood pressure include the following activities. Elevated
arterial pressure increases glomerular capillary blood pressure, which
increases the GFR. Higher GFR leads to higher luminal concentrations
of Na+ and Cl– in the TAL of the nephron, which are monitored by
cells of the macula densa. Increased ion levels in the lumen cause
these cells to release ATP, adenosine, and other vasoactive
compounds that trigger contraction of the afferent arteriole, which
lowers glomerular pressure and decreases the GFR. This lowers
tubular ion concentrations, which turns off the release of
vasoconstrictors from the macula densa (Mescher, 2013).
Decreased arterial pressure leads to increased autonomic
stimulation to the JGA as a result of baroreceptor function, including
local baroreceptors in the afferent arteriole, possibly the JG cells
themselves. This causes the JG cells to release renin, an aspartyl
protease, into the blood. There renin cleaves the plasma protein
angiotensinogen into the inactive decapeptide angiotensin I.
Angiotensin-converting enzyme (ACE) on lung capillaries clips this
further to angiotensin II, a potent vasoconstrictor that directly raises
systemic blood pressure and stimulates the adrenals to secrete
aldosterone. Aldosterone promotes Na+ and water reabsorption in the
distal convoluted and connecting tubules, which raises blood volume
to help increase blood pressure. The return of normal blood pressure
turns off secretion of renin by JG cells (Mescher, 2013).
Collecting Ducts
The last part of each nephron, the connecting tubule, carries the
filtrate into a collecting system that transports it to a minor calyx and
in which more water is reabsorbed if needed by the body. Connecting
tubule extends from each nephron and several join together in the
cortical medullary rays to form collecting ducts of simple cuboidal
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epithelium and an average diameter of 40 μm. In the outer medulla
these merge further as larger, straight collecting ducts (of Bellini),
which run to the tips of the medullary pyramids with increasingly
columnar cells and overall diameters reaching 200 μm. In the apex of
the pyramid, several collecting ducts merge further as a papillary
duct which delivers urine to the minor calyx. Running parallel with
the descending and ascending limbs of the loops of Henle and vasa
recta, medullary collecting ducts lie in the area with very high
interstitial osmolarity (Mescher, 2013).
Collecting ducts are composed mainly of pale-staining principal
cells with few organelles, sparse microvilli, and unusually distinct cell
boundaries. Ultrastructurally the principal cells can be seen to have
basal membrane infoldings, consistent with their role in ion transport,
and a primary cilium among the microvilli. The medullary collecting
ducts are the final site of water reabsorption from the filtrate. Principal
cells are particularly rich in aquaporins, the integral membrane pore
proteins that function as specific channels for water molecules, but
here most aquaporins are sequestered in membranous cytoplasmic
vesicles (Mescher, 2013).
Antidiuretic hormone (ADH), released from the pituitary gland as
the body becomes dehydrated, makes collecting ducts more permeable
to water and increases the rate at which water molecules are pulled
osmotically from the filtrate. Upon binding, ADH receptors on the
basolateral cell surface stimulate the movement and insertion of
vesicles with aquaporins into the apical (luminal) membranes,
increasing the number of membrane channels and water movement
through the cells. The high osmolarity of the interstitium draws water
passively from the collecting ducts, concentrating the filtrate. The
water thus saved immediately enters the blood in the vasa recta
(Mescher, 2013).
24
Scattered among the principal cells are variably darker
intercalated cells, or IC cells, with more abundant mitochondria and
projecting apical folds. Intercalated cells, a few of which also occur in
the DCTs, help maintain acid-base balance by secreting either H+ or
HCO3– (Mescher, 2013).
c. What are the possible causes of swollen?

Answer:
The causes of edema in childhood according to the following
physiological changes: (1) reduced oncotic pressure, (2) increased
blood volume, and (3) increased capillary permeability (Hisano et al.,
2015).
1. Reduced oncotic pressure (Hypoproteinemic diseases, Nephrotic
syndrome, Liver cirrhosis, Malnutrition, Protein losing
nephropathy, and Severe burns)
2. Increased blood volume (Cardiovascular diseases Heart failure:
low-output (congestive heart failure); high-output heart failure
(hyperthyroidism, anemia, beriberi), Arteriovenous fistula, Renal
diseases: Acute glomerulonephritis Acute and chronic renal failure,
Idiopathic diseases: Familial idiopathic edema, and Non-familial
idiopathic edema Pregnancy)
3. Increased capillary permeability (Allergic diseases (angioneurotic
edema, aeroallergens, food allergy), Vasculitis (anaphylactoid
purpura, systemic lupus erythematosus, dermatomyositis,
polyarteritis nodosa, scleroderma, Kawasaki disease)).
Synthesis:
1. Edema due to Reduced oncotic pressure
Edema in nephrotic syndrome. Traditionally, the mechanism of
edema formation in nephrotic syndrome has been considered to be due
25
to plasma volume contraction (underfilling edema). Hypoalbuminemia
that results from albuminuria causes reduced oncotic pressure, leading
to transcapillary fluid in the interstitial space. The resulting decrease
in plasma volume affects sodium and water retention in the kidney
through stimulating the activity of RAA and SNS and ADH
secretions. As long as the disequilibrium of the capillary fluid
exchange remains, the retained fluid will continue to accumulate in
the interstitial space resulting in further edema formation. In a
majority of the patients with nephrotic syndrome, edema formation
can be explained by this mechanism (Hisano et al., 2015).
However, there are observations arguing against reduced plasma
and blood volume in the nephrotic syndrome. Some patients with
nephrotic syndrome show increased plasma volume (overfilling),
hypertension and edema In the patients with steroid-induced remission
of minimal change nephrotic syndrome. diuresis and natriurese begin
before hypoalbuminemia is reversed. Patients with nephrotic
syndrome have high plasma renin activity and increased plasma
aldosterone concentration. Especially in minimal change nephrotic
syndrome with low plasma oncotic pressure (Hisano et al., 2015).
However, plasma aldosterone concentrations are usually normal in
children with minimal change nephrotic syndrome. Shapiro et al in
Hisano et al (2015) reported that a negative sodium balance was
induced in the nephrotic patients by administration of the aldosterone
antagonist, spironolactone. However, Brown et al in Hisano et al
(2015) showed that angiotensin converting-enzyme (ACE) inhibitor
could not induce natriuresis in nephrotic patients. It was suggested
that several other factors must play a role in increased sodium
retention. The reduction in plasma volume presumably suppresses
atrial natriuretic peptide (ANP) secretion, which inhibits sodium
resorption in the inner medullary collecting duct (Hisano et al., 2015).
26
Edema in liver cirrhosis. Edema and ascites are major clinical
findings in patients with liver cirrhosis. The pathophysiology of
edema and ascites in liver cirrhosis is related to portal hypertension,
primary or secondary renal sodium retention, and hemodynamic
changes. Three pathophysiological theories have been proposed to
account for the ascites formation and sodium retention in liver
cirrhosis. According to the traditional, classic "underfilling theory,"
the initial event in renal sodium retention is disruption of the Starling
equilibrium within the hepatic sinusoids and splanchnic capillaries
owing to the increased resistance to portal flow, which leads to
increased filtration of fluid into the interstitial space, that is, peritoneal
cavity. Intravascular fluid movement to the interstitial space leads to
reduced plasma volume resulting in increased activity of RAA and
SNS and increased ADH secretion. The RAA actvity is stimulated in
the patients with decompensated cirrhosis and more so in the patients
with hepatorenal syndrome (Hisano et al., 2015).
If this theory were correct, blood volume and cardiac output would
be reduced. However, it is well established that plasma volume and
cardiac output are markedly increased, and peripheral vascular
resistance is markedly reduced in patients with cirrhosis and ascites.
This "underfilling" theory does not correlate with the systemic
hemodynamic abnormalities related to portal hypertension (Hisano et
al., 2015).
The "overflow theory" was proposed in an attempt to explain the
relationship between portal hypertension and hyperdynamic
circulation in the edema formation. The initial event is a primary renal
sodium retention, and not secondary to a reduction in intravascular
volume renal sodium and water retention would result in expanded
plasma volume and increased cardiac output. The existence of portal
hypertension and circulating hypervolemia would accelerate ascites
formation. However, this theory does not explain the reduced
27
resistance of peripheral arteries and arterial hypotension. In addition,
this theory cannot explain the results of events leading to the
development of hepatorenal syndrome (Hisano et al., 2015).
The third theory, the "peripheral arteriolar vasodilation hypothesis"
is that sodium retention in cirrhosis is a secondary event related to an
arterial vascular underfilling. However, in contrast to the classic
"underfilling" theory, the vascular underfilling is not the result of
reduced intravascular volume but rather due to a decrease in
intravascular volume against a disproportionate enlargement of the
arterial vascular compartment secondary to arteriolar vasodilation.
Portal hypertension and resultant splanchnic arteriolar vasodilation
lead to underfilling of the arterial vascular compartment (Hisano et al.,
2015).
The baroreceptors sense this arterial underfilling and stimulate the
activity of RAA and SNS and increase ADH secretion. Renal sodium
and water retention leads to the increase in plasma volume. In the
status of compensated cirrhosis, normalization of circulatory
homeostasis suppresses the activity of neuroendocrinological system
and renal sodium and water retention is normalized. However, in
decompensated cirrhosis, splanchnic arteriolar vasodilation further
increases and then a more intense arterial vascular underfilling ensues
(Hisano et al., 2015).
At this time, the increased intravascular volume is not enough to
maintain circulatory homeostasis. Arterial pressure is maintained by
the persistent stimulation of the RAA, SNS and ADH and the
activation of these systems perpetuates sodium and water retention,
resulting in accumulation of ascites. What dilates the peripheral artery
is not known. Several potential mediators, such as nitric oxide,
glucagon, prostacyclin, potassium channels, endotoxin and cytokines
are considered vasodilators. Nitric oxide synthesis by up-regulation of
gene expression is likely induced in response to shear stress of the
28
vascular wall concomitant with portal hypertension and increased
flow, and nitric oxide causes vasodilation.However, recent studies do
not consistently support this hypothesis. Plasma glucagon
concentration is high in cirrhotic patients and glucagon causes
vasodilation in pharmacological doses; glucagon likely enhances nitric
oxide production in cirrhosis (Hisano et al., 2015).
Prostacyclin is elevated in cirrhosis. Prostacyclin is a systemic
vasodilator and its secretion is stimulated by shear stress of the
splanchnic arterioles. ATP-sensitive potassium channels can cause
vasodilation due to hyperpolarization of vascular smooth muscle cells.
Moreau et al in Hisano et al (2015) found that vasodilation in cirrhotic
rats is dependent on potassium channels.
Edema in severe malnutrition. Undernutrition, marasmus (caloric
deficiency), or marasmus with kwashiorkor (severe-protein
malnutrition) can occur in the same patient. The development of
edema formation in this pathophysiology is due to "underfilling
mechanism" (Hisano et al., 2015).
Edema in protein-losing enteropathy. The hypoalbuminemia
resulting from chronic protein loss gives rise to a contraction of
extracellular volume, allowing the development of edema due to the
“underfilling mechanism” (Hisano et al., 2015).
Edema in severe burns. In burned tissues, plasma fluid shifts into
the interstitial space by the burn-induced increase in vascular
permeability and the consequent extravasation of protein, and water
and protein accumulate in the interstitial space. Hypoproteinemia
leads to a reduction in oncotic pressure in severe burns, and edema
formation develops progressively through the underfilling mechanism
2. Edema formation due to increased blood volume.
The edema formation secondary to increase in blood volume results
from heart failure, acute glomerulonephritis, acute and chronic renal
29
failure and toxemia of pregnancy. The activity of RAA and SNS and
ADH secretion are suppressed in increased blood volume (Hisano et
al., 2015).
Edema in heart failure. The relation between cardiac output and
peripheral arterial vascular resistance, both of which are primary
determinants of the "fullness" of the arterial vascular system, defines
the volume-control system. Basically, heart failure is characterized by
increased blood volume and increased venous pressure. There are two
types of heart failure, such as low-output heart failure (congestive
heart failure) and high-output heart failure (hyperthyroidism, anemia,
beriberi or an ateriovenous fistula). Hormonal and baroreceptor
response to both types of heart failure is quite similar. The low-output
heart failure is characterized by reduced cardiac output and increasing
filling pressures in one or both ventricles. Arterial pressure is
maintained because of an increase in systemic peripheral vascular
resistance (Hisano et al., 2015).
The hemodynamic characteristics of high-output heart failure are
increased cardiac output, low systemic vascular resistance, arterial
hypotension and increased central venous pressure. In the
development of edema from heart failure, the initial event is reduced
effective arterial blood volume, in both lowoutput heart failure and
high-output heart failure. This event stimulates arterial and ventricular
baroreceptor, resulting in activation of SNS and RAA and release of
ADH (nonosmotic secretion) (Hisano et al., 2015).
The low renal perfusion also stimulates secretion of renin from the
juxtaglomerular apparatus. Increased sodium and water retention leads
to edema formation. Prostaglandins are important for maintaining the
systemic hemodynamics in heart failure and increased production of
prostaglandins in the kidney is important in maintaining renal
hemodynamics. In congestive heart failure, plasma prostaglandin E2
30
and prostaglandin 12 concentrations are increased (Hisano et al.,
2015).
The circulating level of ANP is constantly increased in heart
failure. The enhanced ANP release is a physiological response to
counteract the expanded extracellular volume and reduce the increased
afterload of heart failure as a natriuretic factor and a vasodilator.
However, high level of circulating ANP is not capable of exerting
natriuresis because of a resistance to the renal effects of endogenous
ANP in heart failure. The plasma concentration of human brain
natriuretic peptide is also increased in patients with heart failure
Edema in acute glomerulonephritis. In acute glomerulonephritis,
glomerular filtration is reduced by the glomerular capillary obstruction
caused by the immunological injury. The reduced glomerular filtration
results in a fall in the filtered load of sodium and water, leading to
expanded extracellular volume. The hemodynamic characteristics of
this disease are increased blood volume, hypertension and normal or
increased cardiac output. Blood volume expansion increases
peripheral capillary filtration by increasing arterial and venous
pressures. The return of filtered fluid into venules and via lymphatics
is impaired by the high venous pressure. The primary event of edema
formation in acute glomerulonephritis is the increased blood volume
Edema in acute and chronic renal failure. The decline of
glomerular filtration is primarily attributable to edema formation in
acute and chronic renal failure. An abrupt fall in glomerular filtration
in acute renal failure causes an accumulation of sodium and water,
resulting in an increased blood volume, hypertension and edema
formation. There is also a diffuse increase in peripheral capillary
permeability caused by massive tissue injury (Hisano et al., 2015).
31
In the early stages of chronic renal failure, polyuria and polydypsia
are evident. The ability to dilute the urine is well preserved and urine
output does not dminish. Thus, water depletion and sodium wasting
may ensure in the inadvertent restriction of water and sodium intake
during the early stages of chronic renal failure. Edema formation is
uncommon in early chronic renal failure. However, with the
progressive loss of nephrons, the fall in the glomerular filtration of
water and sodium becomes evident. Blood volume is increased,
leading to edema formation and hypertension, especially after an
abrupt increase of salt intake (Hisano et al., 2015).
d. What is the mechanism of swollen around the eyelids and testicles,

especially after awakening, then in face, both the legs and back of
foot?
Answer:
Decrease blood flow to nephron stimulating polkissen to release
renin, renin go to systemic/ gene ral circulation trough renal veins.
And renin will change angiotensinogen to angiotensin I. Angiotensin I
coverted to angiotensin II by angiotensin converting enzyme (ACE) on
endothelial cells or pulmonary circulation. Angiotensin II will work on
glomerulosa zone in suprarenal glands and release aldosterone. Act on
Principal cell on last part of nephron and stimulate Gene-1 and Na +/K+
ATPase planted on basolateral membrane, it throws Na+ cut of cells
and K+ starts accumulating the effect is fluid retension, increase
intracell fluid and Swollen (Shafik, 2012).
e. Why does swollen first comes on the eyelids and the testicles?
Answer:
32
Swelling is a clinically apparent increase in the volume of
extracellular fluid. The presence of swelling first appears around the
eyelids and the testes indicate a generalized edema has occurred.
swelling depends on 2 factors, namely the force of gravity and local
tissue resistance. The swelling first appears around the eyelid, which is
because the swelling that occurs in the case, initially occurs in areas
with low pressure as in the preorbital region. In addition, the preorbital
area consists of a loose connective tissue that many so easily entered
the liquid. The swelling spreads to the testes due to changes in
positions that are affected by the force of gravity, the more time, the
more liquid the gravity increases so the fluid moves downward
(Harrison, 2000).
f. What does the meaning of Ibnu’s complain?

Answer:
Swollen appeared since 5 days ago its mean an Acute symptom,
swollen of a whole of body its means a general edema based on size,
swollen could be devided 2 type, local and general edema, and
Swallon is clinical manifestation of Acute Glomerulonefritis (IDAI,
2012).
g. What are possible disease of Ibnu’s complain?

Answer:
According to Kowalak (2016), the possible disease of Ibnu’s
complain are the following:
1. Kidney disease (Minimal change disease, Focal segmental
glomerulosclerosis, Glomerulonephritis, Nephritic syndrome,
Chronic renal failure).
2. Liver disease (Liver cirrhosis, Hepatitis)
33
3. Congestive heart failure
4. Inflammatory bowel disease
5. Neuroblastoma
6. Sepsis
7. Stevens-Johnson syndrome
8. Hypothyroidism
9. Filariasis
10.Allergic reaction
11.Hereditary angioedema
12.Portal hypertension
13.Severe malnutrition
14.Constructive pericarditis
15.Gastroenteropaty
2. Ibnu also complained of headaches, but no blurry vision and no

dyspnue.
a. What does the meaning of complaining headaches, but blurry
vision does not exist?
Answer:
Headache in this case is clinical manifestation of Hypertension. No
blurry vision and no dispneu maybe for tell us, this is not Emergency
hypertension.
Synthesis:
Hypertensive emergencies encompass a spectrum of clinical
presentations in which uncontrolled blood pressures (BPs) lead to
progressive or impending end-organ dysfunction. In these conditions,
the BP should be lowered aggressively over minutes to hours
(Hopkins, 2017).
34
Neurologic end-organ damage due to uncontrolled BP may include
hypertensive encephalopathy, cerebral vascular accident/cerebral
infarction, subarachnoid hemorrhage, and/or intracranial hemorrhage.
Cardiovascular end-organ damage may include myocardial
ischemia/infarction, acute left ventricular dysfunction, acute
pulmonary edema, and/or aortic dissection. Other organ systems may
also be affected by uncontrolled hypertension, which may lead
to acute renal failure/insufficiency, retinopathy, eclampsia, or
microangiopathic hemolytic anemia (Hopkins, 2017).
With the advent of antihypertensives, the incidence of hypertensive
emergencies in the United States has declined from 7% to
approximately 1% of patients with hypertension. In addition, the 1-
year survival rate associated with this condition has increased from
only 20% (prior to 1950) to a survival rate of more than 90% with
appropriate medical treatment. Nonetheless, despite its relative rarity,
the number of US emergency department (ED) visits for hypertensive
emergency and the rate per million adult ED visits increased more
than two-fold between 2006 and 2013 (Hopkins, 2017).
The most common clinical presentations of hypertensive
emergencies are cerebral infarction (24.5%), pulmonary
edema (22.5%), hypertensive encephalopathy (16.3%), and congestive
heart failure (12%). Other clinical presentations associated with
hypertensive emergencies include intracranial hemorrhage, aortic
dissection, and eclampsia, as well as acute myocardial infarction
(Hopkins, 2017).
The duration and severity of the patient’s preexisting hypertension
(including the degree of BP control) should be evaluated, as well as
the patient's medication history. Details of antihypertensive drug
therapy and compliance, intake of over-the-counter (OTC)
preparations such as sympathomimetic agents, and use of illicit drugs
such as cocaine are important elements of the medication history. In
35
addition, it is important to elicit information about the presence of
previous end-organ dysfunction, particularly renal and
cerebrovascular disease, and any other medical problems (eg, thyroid
disease, Cushing disease, systemic lupus). In female patients,
determine the date of their last menstrual period (Hopkins, 2017).
Patients may complain of specific symptoms that suggest end-
organ dysfunction may be present. Chest pain may indicate
myocardial ischemia or infarction, back pain may denote aortic
dissection; and dyspnea may suggest pulmonary edema or congestive
heart failure. The presence of neurologic symptoms may include
seizures, visual disturbances, and altered level of consciousness and
may be indicative of hypertensive encephalopathy (Hopkins, 2017).
The physical examination should assess whether end-organ
dysfunction is present. BP should not only be measured in both the
supine position and the standing position (assess volume depletion),
but it should also be measured in both arms (a significant difference
may suggest aortic dissection). The presence of new retinal
hemorrhages, exudates, or papilledema suggests a hypertensive
emergency. Evaluate for the presence of heart failure, which may be
indicated jugular venous distention, crackles on auscultation, and
peripheral edema. Central nervous system (CNS) findings may
include changes in the patient's level of consciousness and visual
fields, and/or the presence of focal neurologic signs. Abdominal
masses or bruits may be noted (Hopkins, 2017).
b. What are possible causes of headaches?

Answer:
Because the brain is insensate, headache is due to the stimulation of
pain-sensitive nerve fibers in large cerebral arteries and veins, the
periosteum of the skull, the muscle and skin of the scalp, the sinus
36
mucosa, the temporomandibular joint, the teeth, or the gingiva (Lopez,
2017).
Headaches are grouped on the basis of etiology, facilitating proper
evaluation and treatment. The Etiology of headaches according to
Lopez (2017) are the following:
 Migraine is the most common type of primary headaches. The
mediators create neurogenic inflammation, including local rupture
of the blood-brain barrier, and trigger vasodilatation, further
stimulating the trigeminal nerve terminals that can cause migraine.
 Tension-type headache. The causes of tension-type headache are
still poorly understood. A combination of muscular factors,
abnormal pain-perception mechanisms, and central emotional
abnormalities exist, all possibly linked to brain-stem serotonergic
interneurons. Furthermore, central and peripheral sensitization is
involved. Contrary to common belief, the relevance of muscle
contraction itself is marginal, especially in the chronic form.
 Posttraumatic headache
 Sinus headache (Acute or chronic sinusitis)
 Benign intracranial hypertension (pseudotumor cerebri) is caused
by the expansion of one or more of the intracranial fluid spaces,
such as the vasculature, the extracellular fluid compartment, or the
cerebrospinal fluid (CSF) space. Several drugs, such as
tetracycline, minocycline, penicillin, gentamicin, oral
contraceptives, steroids, indomethacin, thyroid hormone, and
lithium carbonate, may be inciting agents.
 Other causes (Headache related to meningeal irritation may be
caused by infection (meningitis), inflammation (eg, from a tumor),
or hemorrhage (eg, from vascular malformation or malignant
hypertension).
In this case, the possible causes of headache which is complained

by Ibnu is hypertension.
37
c. What is mechanism of headache in the case?
Answer:
An infection of the skin by streptococcus B haemolytic secrete
antigen in the form of nephritik associated plasminreseptor (NAPlr and
streptococcus pyrogenie exotoxin B (SPEB) activation of the immune
system (anti NAPlr) that is dissolved in the blood and settles on the
basement membrane glomerulus, followed by infiltration of
lymphocytes and macrophages secrete cytokines causing inflammation
of the glomurulus so that renal blood flow decreases and glomerular
filtration rate (GFR) decrease (hypoperfusion) which activates the
renin-angiotensin system, angiotensin II, which is vasoconstriction of
peripheral, angiotensin II will increase stimulus cortex (adrenal) to
release aldosterol resulting in water and salt retention that leads to
hypervolemia and then hypertension that causes headaches in cases.
d. What does the meaning of shortness of breath do not exist?

Answer:
The meaning of shortness of breath do not exist is the causes of the
swollen is not caused by the cardiorespiratory system which dyspneu is
the most common symptoms.
3. Urine volume about one glass per days and red like water meat wash.
a. Why does the urine looked like water of meat wash?
(Pathophysiology)
Answer:
Urine looked like water of meat wash called hematuria. Generally,
hematuria is defined as the presence of 5 or more red blood cells
(RBCs) per high-power field in 3 of 3 consecutive centrifuged
38
specimens obtained at least 1 week apart. Hematuria can be either
gross (ie, overtly bloody, smoky, or tea-colored urine) or microscopic.
It may also be either symptomatic or asymptomatic, either transient or
persistent, and either isolated or associated with proteinuria and other
urinary abnormalities (Gulati, 2017).
The etiology and pathophysiology of hematuria vary. For instance,
hematuria of glomerular origin may be the result of a structural
disruption in the integrity of glomerular basement membrane caused
by inflammatory or immunologic processes. Chemicals may cause
toxic disruptions of the renal tubules, whereas calculi may cause
mechanical erosion of mucosal surfaces in the genitourinary tract,
resulting in hematuria (Gulati, 2017).
Synthesis:
Poststreptococcal glomerulonephritis follows infection with only
certain strains of streptococci, designated as nephritogenic. The
offending organisms are virtually always group A streptococci. Acute
poststreptococcal glomerulonephritis (APSGN) follows pyodermatitis
with group A streptococci M protein types 47, 49, 55, 2, 60, and 57
and throat infection with streptococci M types 1, 2, 4, 3, 25, 49, and
12 (Geetha, 2016).
Although many morphologic, clinical, and serologic features
suggest that APSGN is an immune complex disorder, the precise
nature of the antigen-antibody interaction is undefined. APSGN is
believed to be an immune-mediated disease, in which an immune
complex containing a streptococcal antigen is deposited in the affected
glomeruli. The size of glomerular basement membrane (GBM) pores
and the molecular size of the streptococcus-Ig complex are also
important determinants (Geetha, 2016).
The molecular size of the streptococcus-Ig complex is about 15 nm
(10 nm for streptococcus group A and 5 nm for immunoglobulin). The
39
GBM pore sizes in children and adults are 2-3 nm and 4-4.5 nm,
respectively. Therefore, the immune complex molecule can be more
easily rodded into the glomerulus in children than in adults and, thus,
may explain the increased frequency of APSGN in children compared
to that in adults (Geetha, 2016).
The two antigens isolated from nephritogenic streptococci are
under investigation in APSGN. These include the cationic cysteine
protease streptococcal pyrogenic exotoxin B and nephritis-associated
streptococcal plasmin receptor, which is a plasmin-binding protein
with glyceraldehyde phosphate dehydrogenase (also known as
presorbing antigen or PA-Ag). These fractions have an affinity for
glomeruli and have been shown to induce specific, long-lasting
antibody responses in biopsy specimens from patients with APSGN
(Geetha, 2016).
The relevance of exotoxin B and glyceraldehyde phosphate
dehydrogenase was evaluated in the same renal biopsy and serum
samples of patients with well-defined APSGN. Glomerular deposits of
and antibody response to exotoxin B were more consistently present in
APSGN than were deposits of and antibody response to
glyceraldehyde phosphate dehydrogenase (Geetha, 2016).
Antibodies to exotoxin B and PA-Ag are elevated in the majority of
patients with APSGN. Intravenous injections of PA-Ag produce acute
glomerulonephritis in animals. Antibodies to PA-Ag are found in 30
of 31 patients with APSGN but are low or absent in those with
uncomplicated streptococcal infection or in patients with rheumatic
fever (Geetha, 2016).
PA-Ag is also known to activate the alternate pathway of the
complement cascade, which happens to be preferentially activated in
persons with APSGN. The observation that some patients may only
have C3 deposition may relate to this mechanism. In addition to
streptococcal antigens, rheumatoid factor, cryoglobulins, and
40
antineutrophil cytoplasmic serum antibodies are present in some of
these patients. The pathogenic significance of this autoimmune
response is not defined (Geetha, 2016).
There are also host susceptibility factors. In one study, HLA-
DRB1*03011 was reported to be found at a significantly higher
frequency in 32 unrelated patients with APSGN as compared to 380
healthy individuals (Geetha, 2016).
b. How much is the normal urinary volume production in a day?

Answer:
The normal urinary volume production in a day is 600-1000 ml
(See Table 1 below).
Oligouri :100-600 ml/24 jam,
Anuri : 100ml/ 24 jam.
In this case, the patient has suffers oligouri
Table 1. Normal Urinary Volume

No. Age Urin Volume
1. Newborn day 1-2 30-60 ml
2. Newborn day 3 – 10 100 - 300 ml
3. Day-10 – 2 months 250 - 450 ml
4. 2 months – 1 years 400 – 500 ml
5. 1-3 years 500 - 600 ml
6. 3-5 years 600 – 700 ml
7. 5-8 years 650 – 700 ml
8. 8-14 years 800 - 1400 ml
(Richard, 2011)
41
c. What does the meaning of urine volume about one glass per day
and red like water meat wash?
Answer:
The meaning of urine is only 1 cup per day is ibnu experiencing
oligouria.
Synthesis:
Oligouria is a state where urine output is less than 1ml/kgBW/hour.
This symptom is closely related to loss of concentration and dilution
ability, where urine osmolality persists approximately the same as
plasma, which would indicate that the function of dilution and renal
concentration is no longer present so that this loss is partly due to
damage to the countercurrent mechanism, but the more important
cause is the destruction of the nephron which results in decreased urine
volume. Oliguria is one of the clinical signs of decreased renal
function or arising acute renal failure (Behrman, 2000: 1805).
d. What are possible disease of oliguria and hematuria?

Answer:
According to Lestariningsih (2014) the possible causes of hematuria
are:
 Glomerulonefritis primer dan sekunder
 Acute Pielonefritis
 Nefrolitiasis
 cystitis
 Uretritis
 Sickle cell disease
According to Devarajan (2017) the causes of acute oliguria can be
grouped into three categories:
42
 Prerenal (Perinatal asphyxia, Respiratory distress syndrome,
Hemorrhage - Eg, maternal antepartum, twin-twin transfusion, and
intraventricular, Hemolysis, Polycythemia, Sepsis or shock,
Congenital heart disease, Dehydration, Drugs - Eg, indomethacin,
maternal nonsteroidal anti-inflammatory drugs (NSAIDs), and
maternal ACE inhibitor).
 Renal or intrinsic (Acute tubular necrosis - Eg, prolonged prerenal
failure, Glomerulonephritis, Interstitial nephritis, vascular - Eg,
hemolytic-uremic syndrome and vasculitis, Exogenous toxins - Eg,
aminoglycosides, amphotericin B, cyclosporine, chemotherapy,
heavy metals, and contrast agents, Endogenous toxins - Eg,
hemoglobin, myoglobin, and uric acid, Transplant rejection).
 Post renal (Nefrolithiasis, Bladder outlet obstruction-eg: posterior
urethral valves and meatal stenosis).
On the cases, the possible causes of hematuria and oligouria is

Glomerulonephritis
4. Two weeks before appears of swollen, Ibnu suffered from scabs in the
area of legs. Ibnu didn’t seek treatment and his scabs dry themselves.
The symptoms of this disease first experienced. No family suffers from
this disease.
a. What is the meaning of two weeks before the swollen, ibnu
suffered scabs in the area of legs?
Answer:
Acute glomerulonephritis is preceded by infection with acute
respiratory tract or skin infection (piodermi) with period latent 1-2
weeks on ARD or 3 weeks on pioderma (IDAI, 2012).
Impetigo seldom progresses to systemic infection,
although poststreptococcal glomerulonephritis is a rare complication
43
with GABHS infection only.Certain serotypes of GABHS (eg, types
49, 55, 57, 59) are associated with impetigo and acute
glomerulonephritis (Lewis, 2016).
Synthesis:
Impetigo is an acute, highly contagious gram-positive bacterial
infection of the superficial layers of the epidermis. Skin lesions such
as cuts, abrasions, and chickenpox can also become secondarily
infected (impetiginized) with the same pathogens that produce classic
impetigo (Lewis, 2016).
Impetigo occurs most commonly in children, especially those who
live in hot, humid climates. The name is believed to be derived from
the Latin impetere (to assail). Impetigo occurs in 2 forms: bullous and
nonbullous, as shown in the photographs below. Nonbullous impetigo
is the more common form, constituting approximately 70% of
impetigo cases. It tends to affect skin on the face or extremities that
has been disrupted by bites, cuts, abrasions, other trauma, or diseases
such as varicella (Lewis, 2016).
b. How is the microbiology of the bacteria that cause the scabs in the
area of legs?
Answer:
The microbiology of the bacteria that cause the scabs in the area of
legs are Staphylococcus aureus (the predominant organisms, 43% of
infected leg ulcers to 88% of non-infected leg ulcers), Staphylococcus
epidermidis (14% of venous ulcer specimens and 20.6% of diabetic
foot ulcers (DFUs)) (Jones, 2005).
Pseudomonas aeruginosa (7–33% of ulcers), aerobic species
including Escherichia coli, Enterobacter cloacae, Klebsiella species,
Streptococcus species, Enterococcus species and Proteus species
(Jones, 2005).
44
Synthesis :
The microflora of leg and foot ulcers is usually polymicrobial and
recent studies using molecular techniques have emphasized the
complex ecology of these wounds. Using conventional techniques, the
mean number of bacterial species per ulcer has been found to range
from 1.6 up to 4.4. Hansson et al. observed that 86% of ulcers with no
clinical signs of infection contained more than one bacterial species
(Jones, 2005).
Staphylococcus aureus and coagulase-negative staphylococci have
been the predominant organisms isolated from both prospective,
purpose-collected samples and retrospective analysis of clinical
investigations. S. aureus has been reported in frequencies varying
from 43% of infected leg ulcers to 88% of non-infected leg
ulcers whereas Staphylococcus epidermidis has been reported in 14%
of venous ulcer specimens and 20.6% of diabetic foot ulcers (DFUs).
Pseudomonas aeruginosa is another frequently identified organism
and has been found in 7–33% of ulcers. A number of other aerobic
species have also been reported, including Escherichia coli,
Enterobacter cloacae, Klebsiella species, Streptococcus species,
Enterococcus species and Proteus species. This is by no means an
exhaustive list, but is illustrative of the range of aerobic bacteria that
exist in chronic wounds (Jones, 2005).
In addition to aerobes, anaerobic organisms are frequently
identified in wounds, albeit with considerable variation. Trengove et
al. found obligate anaerobes in one-quarter of chronic leg ulcer
samples, whilst Ge et al. found they constituted only 6% of DFU
wound isolates. However, a focused study by Bowler & Davies found
anaerobes in 73% of non-infected leg ulcers and 82% of infected leg
ulcers (Jones, 2005).
45
The most common isolates found in both the infected and non-
infected leg ulcers were Peptostreptococcus species and pigmented
and non pigmented Prevotella/Porphyromonas species. Finegoldia
magna (previously classified as Peptostreptococcus magnus) was
found by Hansson et al. to be present in 19.6%, and Peptoniphilus
asaccharolyticus in 9.8% of non-infected venous leg ulcers.
Kontiainen & Rinne16 found that clinical swabs sent for analysis,
presumably from infected or assumed infected wounds, yielded
obligate anaerobic rods (mainly Bacteroides species) from 12% of
ulcers and anaerobic cocci (peptostreptococci) from 8% (Jones, 2005).
c. What is the correlation between the scabs in the area of legs with
the swollen that was suffered by Ibnu?
Answer:
Ibnu suffered poststreptococcal-infection.
d. What is meaning of these symptoms are the first experienced?

Answer:
This symptom are the first experience means there is suggest that
the disease is acute phase not a recurrence or exarcebation of another
disease are suffered befeore.
e. What is meaning of no family suffers the same?
Answer:
Family history no one experienced the same complaint, the
meaning of illness experienced by Ibnu is not a disease caused by
heredity. It can also rule out the differential diagnosis of Alport
syndrome, a hereditary disease (hereditary nephritis) caused by gene
abnormalities by chromosome X (Zheng et al., 2009).
5. Physical Examination :
Vital Signs : BP 140/90 mmHg, weight 28 kg, height 113 cm.
46
Specific Circumstances:
Head : edema palpebra (+)/(+), pale conjunctiva (+)
Chest : Lung : vesicular (+) normal, ronki (-), wheeze (-)
Heart : heart sound I / II normal, noisy (-)
Abdomen : convex, limp, shifting dullness (+), tenderness (-),
Extremities : pitting (+)/(+) edema, edema dorsum pedis (+)/(+)
a. How does the interpretations of physical general findings?
Answer:
Table 2. Interpretation of Physical General Findings
Examination Case Normal Interpretation
General Compos mentis Compos mentis Normal
Moderate illnes healthy Abnormal
Condition
Body weight 28 Category from cdc: Abnormal
kg Obesitas : >120 (obesity)
Over weight : >110
Height 113 cm caused by
Normal : >90
Nutrition less: 70-90 accumulation
Malnutrion: 70
according to the of fluid in
CDC table body
obtained,
=body weight
case / body
weight ideal from
cdc x 100%
= 28/20 x 100%
= 140
Vital signs BP 140/90 mmHg  Normal < 90th Grade II
hypertension
percentile
 Prehypertension
90th to <95th
percentile or
>120/80 mmHg
 Stage 1
47
hypertension 95th
to ,99th percentile
plus 5 mmhg
 Stage 2
hypetension >99th
percentile plus 5
mmHg
Pulse 96x/menit 60 – 100 x/menit Normal
RR 28x/mnt < 2 bulan < 60 Normal
2-12 bulan < 50
1-5 tahun < 40
> 5 tahun < 30
Temp 36,8oC 36,8 – 37,2 oC Normal
b. How to determine hypertension in children, including the grades?

Answer:
Hypertension in the pediatric population is now commonly
observed. Hypertension is known to be a major cause of morbidity and
mortality in the United States and in many other countries, and the
long-term health risks to children with hypertension may be
substantial. In the United States, extensive normative data on blood
pressure (BP) in children are available (NIH, 2004).
The Task Force on Blood Pressure Control in Children,
commissioned by the National Heart, Lung, and Blood Institute
(NHLBI) of the National Institutes of Health (NIH), developed
standards for BP by using the results of 11 surveys of more than
83,000 person-visits of infants and children (including approximately
equal numbers of boys and girls) (NIH, 2004).
48
The percentile curves were first published in 1987 and describe
age-specific distributions of systolic and diastolic BP in infants and
children, with corrections for height and weight (NIH, 2004).
The Third Report of the Task Force, published in 1996, provided
further details regarding the diagnosis and treatment of hypertension
in infants and children. In 2004, the Fourth Report added normative
data and adapted the data to growth charts from the Centers for
Disease Control and Prevention (CDC) for 2000 (NIH, 2004).
In accordance with the recommendations of the Task Force, BP is
considered normal when the systolic and diastolic values are less than
the 90th percentile for the child’s age, sex, and height. The Fourth
Report introduced a new category, prehypertension, which is
diagnosed when a child’s average BP is above the 90th percentile but
below the 95th. Any adolescent whose BP is greater than 120/80 mm
Hg is also given this diagnosis, even if the BP is below the 90th
percentile. This classification was created to align the categories for
children with the categories for adults from the recommendations of
theSeventh Report of the Joint National Committee on Prevention,
Detection, Evaluation, and Treatment of High Blood Pressure (JNC-7)
(NIH, 2004).
Stage I hypertension is diagnosed if a child’s BP is greater than the
95th percentile but less than or equal to the 99th percentile plus 5 mm
Hg. Stage II hypertension is diagnosed if a child’s BP is greater than
the 99th percentile plus 5 mm Hg. It may be categorized as
prehypertension if the BP is between 90th to 95th percentile (NIH,
2004).
If the systolic and diastolic pressures give rise to a discrepancy
with respect to classification, the child’s condition should be
categorized by using the higher value. Table 2 (see below) serves as a
guide to the practicing physician. Full blood pressure tables for
children and adolescents are available from the NHLBI (NIH, 2004).
49
c. How does the interpretations of specific circumstances?
Answer:
50
Table 3. Specific Circumstances Interpretation
Spesific
Case Normal Interpretation
Circumstances
Head palpebra edema palpebra edema Abnormal
+/+, -/-,  palpebra
anemic anemic edema
conjungtivas +/ conjungtivas -/- because
+ edema
moves to
low
interstitial
pressure as
in
preorbital
area
 anemic
conjungtiva
s cause
red blood
cells go out
with urine
Neck No lymp gland No lymp gland Normal
enlargement enlargement
Chest Pulmo: sound pulmo and heart Normal
vesicular, no within normal
rhales, no limits
wheezing
Heart: heart
sound I/II
normal no
murmur
Abdomen Buldging, Flat, shifting Abnormal
tender, with dullness (-) (because fluid
shifting accumulates in
dullness, liver abdominal
and lien are not cavity)
palpable,
normal bowel
sound
Exstremity pitting edema +/ pitting edema -/-, Abnormal
51
+, dorsum pedis dorsum pedis (because fluid
edema +/+ edema -/- to extremities
d. How does mechanisms of the abnormal physical general findings
and specific circumstances?
Answer:
Moderate illnes
Retention of H2O and Sodium → increased blood volume → increased
hydrostatic pressure → edema moves to low interstitial pressure as in
the preorbital region → spongy on eyelid → spreads to other loose
connective tissue → whole body pussy (moderate illnes) (Price, Sylvia
Anderson, 2005)
Abnormal weight
Retention of H2O and Sodium → increase blood volume → increased
hydrostatic pressure → edema moves to low interstitial pressure as in
preorbital region → fluid accumulation in body → abnormal weight.
(Price, Sylvia Anderson, 2005)
52
Palpebra edema, bulging, tender with shifting dullness, dorsum
pedis edema
Streptococcal infection → Immune complex (Antigen-Antibodies) →
circulates and precipitates in the glomerulus → pre-streptococcus
antibodies that have previously formed bind to a molecule mimicry of
a renal protein that resembles the antigen Streptococcus → autoantigen
reacts with circulating antibodies → inflammation of the glomeruli →
decreased glomerular filtration rate → renal hypoperfusion →
decreased renal arteriole and systemic pressures → activation of
juxtaglomerular apparatus → removal of renin → angiotensinogen
conversion into angiotensin 1 → conversion of angiotensin 1 to
angiotensin 2 with the help of Angiotensin Converting Enzyme (ACE)
→ aldosterone secretion → salt and water retention → hypervolemia
→ increased intravascular hydrostatic pressure → fluid spur to
interstitial space → edema → the preorbital region is composed of
loose connective tissue and has a low pressure → palpebral edema →
then due to gravity Abdominal bulging, tender with shifting dullness,
dorsum pedis edema.
Hypertension
Streptococcal infection → Immune complex (Antigen-Antibodies) →
circulates and precipitates in the glomerulus → preformed anti-
streptococcal antibody binds to a molecule mimicry of a renal protein
resembling the antigen Streptococcus → autoantigen reacts with
circulating antibody → inflammation of the glomerulus → decreased
glomerular filtration rate → renal hypoperfusion → decreased renal
arteriole and systemic pressures → activation of juxtaglomerular
apparatus → removal of renin → angiotensinogen conversion into
angiotensin 1 → angiotensin 1 conversion into angiotensin 2 with the
help of Angiotensin Converting Enzyme (ACE) → aldosterone
secretion → salt and water retention → peripheral resistance →
53
increased intracellular volume → cardiac output increases → increased
work of the heart → hypertension.
Anemic conjungtiva
Streptococcus infection → Immune complex (Antigen-Antibodies) →
circulates and precipitates in glomerulus (sub-endothelial and
mesangium) → chemotaxis in inflammatory mediators and
complement → damage to glomerulus (in basal membrane) →
increased permeability of glomerular capillary walls → erythrocytes
much goes into → glomerulus is excreted with urine → hematuria →
anemia → blood is preferred to vital organs → anemic conjungtiva.
e. What is meaning of lung and heart-specific examination results

within normal limits?
Answer:
To exclude diseases of the lungs and heart disorders, and also show
that there has been no complication in Ibnu, where the complications
of GNAPS itself that are pulmonary edema and hypertensive
encephalopathy.
6. What disturbances might happen in this case?

Answer:
1. Kidney disease:
a. Glomerulonephritis chronicles acute exacerbations
This disorder is important to be distinguished from GNAPS
because the prognosis is very different. It is important to think of
this disease if anamnesis there is a previous kidney disease and a
latent period that is too short, usually 1-3 days. In addition to the
54
developmental disorders, anemia and urea are clearly increased
the time the onset of symptoms of nephritis can help the
diagnosis.
b. Kidney disease with hematuria manifestations
These diseases may include focal glomerulonephritis,
hereditary nephritis (Alport syndrome), IgA-IgG nephropathy
(Maladie de Berger) and benign recurrent haematuria. Generally,
this disease is not accompanied by edema or hypertension. The
occurring microscopic haematuria usually recurs and coincides
with an airway infection without a latent period or if there is very
short duration.
c. Rapidly progressive glomerulonephritis (RPGN)
RPGN is more common in adults than in children. This
disorder is often difficult to distinguish from GNAPS especially
in the acute phase in the presence of oliguria or anuria. ASO
titers, AH ase,
2. Systemic diseases
Some diseases that need to be diagnosed of appeal are Henoch-
Schöenlein purpura, erythematosus and subacute bacterial
endocarditis. These three diseases can show symptoms of acute
nephritic syndrome, such as haematuria, proteinuria and other
sedimentary disorders, but in negative throat swabs and normal ASO
titers. In the HSP can be found purpura, abdominal pain and
arthralgia, whereas in acute glomerulonephritis no such symptoms. In
SLE there are skin abnormalities and positive LE cells on blood tests,
which are absent in acute glomerulonephritis, whereas in SBE there is
no edema, hypertension or oliguria. Renal biopsy may confirm the
difference with acute glomerulonephritis with diffuse histologic
abnormalities, whereas the three diseases are generally focal.
3. Infectious diseases
55
Acute glomeruonephritis may also occur after certain bacterial or
viral infections other than by Group A ß-hemolytic streptococci.
Some literature reports acute glomerulonephritis symptoms that arise
after morbili virus infection, parotitis, varicella, and ECHO virus. The
differential diagnosis with acute glomerulonephritis is by looking at
the underlying disease.
7. What investigations are needed to diagnose this case?

Answer:
 Complete Blood Count
 Kidney function test
 Immunologic test
 Kidney ultrasound
 Histologic examination of renal biopsy
 ECG
 Photo thorax
 Serum electrolytes
 Serological examination
 Culture and drug resistance
- Routin blood :Hb 8.0 g/dl, leucocytes count 18.500/mm3, platelets

count450.000/mm3, LED 98 mm/hr
- Urinalysis :Colors ( bahasa lab biasa nya cm bilang keruh), proteinuria
(+3), erythrocyte count 30-50 cells/hpf leukocyte count 2-5 cells/ hpf,
cylinders (+)
- protein and renal functions :Total protein 5.2 g/dl, albumin 1.2 gr/dl,
globulin 4 gr/dl, ureum 40 mg/dl, creatinine 2.0 mg/dl, cholesterol 180
mg / dl.
- Immunology : ASTO 420 IU, CRP (+), titer C3: 60, titer C4: within
normal limit
56
- skin scrapings Culture: Streptococcus B hemolytic is growd
Table 4. Laboratory Findings Interpretation

No. Normal Range Interpretation
1. Regular Hb 8,0 g/dl 13,5-17,5 g/dl Anemia
Leucocytes 4.500-11.000/mm3 Infection
blood
18.500/mm3
Platelets 150.000- Normal
450.000/mm3 450.000/mm3
ESR 98 mm/hr 0-22 mm/hr Increased
2. Urinalysis Colors like meat Yellow (pale to Hematuria
wash water dark)
proteinuria (+3) (-) Proteinuria
erythrocyte 30- < 2/hpf Increased
50 cells/hpf
leukocyte 2-5 < 2-5/hpf Normal
cells/ hpf
cylinders (+) (-) Hematuria
3. Blood Total protein 5.2 6,0-8,0 g/dl Decreased
chemistry g/dl,
Albumin 1.2 3,5-5,5 gr/dl Decreased
gr/dl
Globulin 4 gr/dl 2,5-3,5 gr/dl Increased
Ureum 40 mg/dl 15-40 mg/dl Normal
Creatinine 2.0 0,7-1,3 mg/dl Increased
mg/dl
Cholesterol 180 < 200 Normal
mg / dl.
4. Immunology ASTO 420 IU < 200
CRP (+)
Titer C3: 60 83-177 mg/dl Decrease
Titer C4: normal 15-45 mg/dl Normal
5. Cultured skin Found Abnormal
scrapings Streptococcus B
hemolytic.
8. What disturbances are most likely to occur in this case?

Answer:
57
Acute Nephritic Syndrome due to Acute Poststreptococcal
Glomerulonephritis.
9. How is the classification of Acute Nephritic Syndrome?

Answer:
Diseases or conditions classified into SNA (acute nephritic syndrome)
according to IDAI (2012), include:
- Acute exacerbation chronic glomerulonephritis
- Kidney disease with hematuria manifestations
- Focal glomerulonephritis
- Hereditary nephritis (Alport syndrome)
- IgA-IgG nephropathy (Maladie de Berger)
- Rapid progressive glomerulonephritic
Systemic diseases
- Benign recurrent hematuria
- Purpura Henoch-Schöenlein (HSP)
- Systemic lupus erythematosus (SLE)
10. How is the epidemiology of Acute Nephritic Syndrome? (APSGN)

Answer:
This condition typically affects children aged 2-12 years. A large series
reported that 5% are younger than 2 years and 10% are older than 40 years
(Gheetha, 2016).
Clinical cases of APSGN are twice as common in males than in

females. If subclinical disease is considered, both sexes are affected
equally. The familial incidence rate is nearly 40%, but no genetic marker
has been identified. No racial predilection is recognized (Gheetha, 2016).
In US the incidence of clinically detectable glomerulonephritis during

an epidemic is up to 10% of children with pharyngitis and 25% of children
with impetigo. A systematic review by Jackson et al demonstrated
58
significant variation in the global incidence of APSGN, with the highest
incidence of 239 per 10,000 in Australian Aborigines and lowest incidence
of 0.04 in 100,000 in an Italian study of people younger than 60 years.
Among epidemic infections with nephritogenic streptococci, the apparent
clinical attack rate is 10-12% (Gheetha, 2016).
Synthesis:
Frequency
United States
The incidence of clinically detectable glomerulonephritis during an

epidemic is up to 10% of children with pharyngitis and 25% of children
with impetigo. One study reported a change in the epidemiology of
APSGN and found that pharyngitis has replaced impetigo as the
predominant cause of APSGN (Gheetha, 2016).
International
APSGN can occur sporadically or epidemically. The incidence seems to
be decreasing in the United States and Europe, but sporadic cases of the
disease continue to be reported from all over the world. The prevalence of
nephritis varies considerably among persons with sporadic infections with
nephritogenic streptococci. The reason for this variability is not known
(Gheetha, 2016).
A systematic review by Jackson et al demonstrated significant variation
in the global incidence of APSGN, with the highest incidence of 239 per
10,000 in Australian Aborigines and lowest incidence of 0.04 in 100,000
in an Italian study of people younger than 60 years (Gheetha, 2016).
Epidemic poststreptococcal glomerulonephritis occurs mainly in
developing countries in areas such as Africa, the West Indies, and the
Middle East. Reasons for this changing epidemiology relate to the
59
nutritional status of the community, the more liberal use of antibiotic
prophylaxis, and possibly the change in the nephritogenic potential of
streptococci. Among epidemic infections with nephritogenic streptococci,
the apparent clinical attack rate is 10-12% (Gheetha, 2016).
Mortality/Morbidity
Early death is extremely rare in children (< 1%) but is significantly

more common in adults (25%). This is secondary to congestive heart
failure and azotemia. Congestive heart failure is more common in adults
(43%) than in children (< 5%). Nephrotic-range proteinuria is also more
common in adults (20%) than in children (4-10%). Approximately 83% of
adults have azotemia, compared with 25-40% of children (Gheetha, 2016).
Six cohort studies report case fatality rates from APSGN, with three
revealing a case fatality rate of 0%, two studies from India reporting a case
fatality rate of 1.4% and 2%, and one study from Turkey reporting a case
fatality rate of 0.08% (Gheetha, 2016).
The long-term prognosis of children with APSGN has been the subject
of several studies. Pooled data of studies published prior to 2000 with 5- to
18-year follow-up indicate abnormal urinalysis in 17.4%, proteinuria in
13.8%, hypertension in 13.8%, and azotemia in 1.3%. A study from
Australia demonstrated that APSGN can add to the burden of chronic
kidney disease (Gheetha, 2016).
Race
No racial predilection is recognized (Gheetha, 2016).
Sex
Clinical cases of APSGN are twice as common in males than in

females. If subclinical disease is considered, both sexes are affected
equally. The familial incidence rate is nearly 40%, but no genetic marker
has been identified (Gheetha, 2016).
60
Age
This condition typically affects children aged 2-12 years. A large series
reported that 5% are younger than 2 years and 10% are older than 40 years
(Gheetha, 2016).
11. How does the comprehensive management for this case? (promotive,
preventive, curative and rehabilitative)?
Answer:
1. Rest
Resting in bed especially when complications occur that usually
occur within the first week of GNAPS disease. After the acute phase,
no bed rest is recommended, but no such activity is allowed before
illness. The duration of treatment depends on the state of the disease.
Formerly recommended prolonged bed rest for months with the reason
proteinuria and microscopic hematuria have not disappeared. Now
more progressive, the patient is discharged after 10-14 days of
treatment provided there is no complication. If still encountered
urinary laboratory abnormalities, then performed further observations
at the time of treatment of the road. Excessive rest in bed causes the
child can not play and away from his friends, so it can provide
psychological burden (IDAI, 2012).
2. Diet
The amount of salt given should be noted. When severe edema,
given food without salt, whereas if the edema is light, salt
administration is limited to 0.5-1 g / day. Protein is limited when the
ureum level rises, ie as much as 0.5-1 g / kgb / day. The fluid intake
should be well calculated, especially in oliguria or anuria patients, ie
the amount of fluid intake must be balanced with expenditure, means
61
fluid intake = urine amount + insensible water loss (20-25 ml / kgbb /
day) + the amount of fluid requirement in each temperature rise from
normal (10 ml / kgb / day) (IDAI, 2012).
3. Antibiotics
GNAPS antibiotics have been controversial today. One party only
gives antibiotics when culture of the throat or skin is positive for
streptococcus, whereas others give it regularly with the reason that
negative cultures have not been able to exclude streptococcal
infection. Negative cultures may occur due to antibiotics before
hospitalization or due to long latent periods (> 3 weeks). Penicillin
class medical therapy is given for eradication of germs, Amoxicillin
50 mg / kgbb divided into 3 doses for 10 days. If there is an allergy to
the penicillin group, can be given erythromycin dose 30 mg / kgbb /
day (IDAI, 2012).
4. Symptomatic
Circulatory Dam
The most important thing in dealing with circulation is fluid
restriction, in other words intake must be in accordance with the
output. If there is severe edema or signs of acute pulmonary edema,
diuretics should be given, eg furosemide, if unsuccessful then
peritoneal dialysis (IDAI, 2012).
Acute renal failure
Important things to note are fluid restriction, adequate calorie
delivery in the form of carbohydrates. In case of acidosis should be
given sodium bicarbonate and if there is hyperkalemia given Ca
glukonas or kayexalate to bind potassium (IDAI, 2012).
5. Referral to paediatric nephrology
12. What will happen if these circumstances are not manage

comprehensively?
Answer:
62
The most common acute complication is hypertension with or without
central nervous system (CNS) manifestations. Anemia is common early in
the disease and is primarily due to dilution, although in 2 instances,
autoimmune hemolytic anemia was documented in the early stages of
APSGN. An occasional patient develops pulmonary edema because of the
marked increase in vascular volume that is present in the early phase of the
disease. Congestive heart failure is rare but has been reported (Bhimma,
2017).
The renal survival of APSGN in the developed world is significantly
worse than in the epidemic form of APSGN seen in the developing world.
A third to two third of patients in the developed world developed chronic
kidney disease that may progress to end-stage kidney disease. These
outcomes may be influenced by the susceptibility of patient in developed
countries, who are usually old and have comorbidities (Bhimma, 2017).
13. Is this disorder can be overcome thoroughly, how the odds?

Answer:
Quo ad Vitam : Dubia ad bonam
Quo ad Fungsionam : Dubia ad bonam
Synthesis:
This disease can heal completely within 1-2 weeks if there is no
complication, so often classified into self limiting disease. Although very
rare, GNAPS may recur (IDAI, 2012).
14. How does the competence of general practitioner for this case?
Answer:
The general practitioner competencies for this case is 3A.
Synthesis:
3A. Non-emergency case
63
General practitioner are able to make clinical diagnoses and provide
preliminary therapy in non-emergency cases, to determine the most
appropriate referral for the next patient's treatment and also able to follow
up after returning from referrals.
15. How does the Islamic point of view of this case?

Answer:
Rasulullah Shallallahu alaihi wassalam said "No Muslim is struck by
disaster, sickness, anxiety or thorns in it but Allah SWT will forgive his
past sins” (H.R Bukhari).
2.6 Conclusion
Ibnu experiences a whole body swelling, grade 2 hypertension, hematuria
and oligouria (Acute Nephritic Syndrome) because suffered Acute Post-
Streptococcal Glomerulonephritis with predisposition factor: immune
hypersensitive (Type III hypersensitivity).
2.7 Conceptual framework

Possible skin infections by streptococcus  (predisposition factor:
immune hypersensitive) create immune complex (Antigen-antibody complex)
 deposited in kidney (glomerulus)  glomerular inflammation  decrease
renal function  Swollen, grade 2 hypertension, hematuria, and oligouria.
64
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Isi Laporan Tutorial Skenario B Blok 15

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Isi Laporan Tutorial Skenario B Blok 15

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CHAPTER I

1.2 Purpose and Objectives

2.1 Tutorial’s Data

2.2 Case Scenario

2.3 Clarification of Terms

2.4 Problem Identification

Picture 1.1 Right Kidney, coronal section

Picture 1.2 Kidneys

External anatomy of the Kidneys

Picture 1.3 Frontal Section of Right Kidney

Internal anatomy of the kidneys

Picture 1.4 Nephrons

Blood and nerve supply of the kidney

Picture 1.5 Blood Supply of Kidneys

Source: Mescher, 2013 (Junqueira’s Basic Histology)

Renal Corpuscles & Blood Filtration

Picture 1.6 Renal Corpuscle

The outer parietal layer of a glomerular capsule consists of a simple

Proximal Convoluted Tubule

Transcellular reabsorption involves both active and passive

Picture 1.8 Nephrons

Picture 1.9 Histology of Nephrons

The loops of Henle and surrounding interstitial connective tissue

Distal Convoluted Tubule & Juxtaglomerular Apparatus

Picture 1.10 Nephrons

c. What are the possible causes of swollen?

d. What is the mechanism of swollen around the eyelids and testicles,

f. What does the meaning of Ibnu’s complain?

g. What are possible disease of Ibnu’s complain?

2. Ibnu also complained of headaches, but no blurry vision and no

b. What are possible causes of headaches?

In this case, the possible causes of headache which is complained

d. What does the meaning of shortness of breath do not exist?

b. How much is the normal urinary volume production in a day?

Table 1. Normal Urinary Volume

d. What are possible disease of oliguria and hematuria?

On the cases, the possible causes of hematuria and oligouria is

d. What is meaning of these symptoms are the first experienced?

b. How to determine hypertension in children, including the grades?

e. What is meaning of lung and heart-specific examination results

6. What disturbances might happen in this case?

7. What investigations are needed to diagnose this case?

- Routin blood :Hb 8.0 g/dl, leucocytes count 18.500/mm3, platelets

Table 4. Laboratory Findings Interpretation

8. What disturbances are most likely to occur in this case?

9. How is the classification of Acute Nephritic Syndrome?

10. How is the epidemiology of Acute Nephritic Syndrome? (APSGN)

Clinical cases of APSGN are twice as common in males than in

In US the incidence of clinically detectable glomerulonephritis during

The incidence of clinically detectable glomerulonephritis during an

Early death is extremely rare in children (< 1%) but is significantly

No racial predilection is recognized (Gheetha, 2016).

Clinical cases of APSGN are twice as common in males than in

12. What will happen if these circumstances are not manage

13. Is this disorder can be overcome thoroughly, how the odds?

15. How does the Islamic point of view of this case?

2.7 Conceptual framework

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